Acute Cerebral Injuries Research Articles

Course of brain damage following malignant hypertension.

Malignant hypertension (MHT) crisis triggers widespread microvascular damage, particularly in the brain. Despite recent MRI evidence highlighting acute cerebral injuries during MHT crises, follow-up data remain scarce. This study seeks to fill this gap by exploring how brain MRI markers evolve following acute MHT crisis management. We conducted a retrospective analysis of brain MRI data from MHT patients admitted to Bordeaux University Hospital between 2008 and 2022. Eligible patients had at least one follow-up MRI. Analysis blinded to clinical data was performed to identify markers of posterior reversible encephalopathy syndrome (PRES), acute stroke, cerebral hemorrhage, and microangiopathy. Out of 149 patients, 47 had follow-up MRIs. Most were male (72.3%) with a mean age of 48.2 ± 10.8 years. The median interval between initial and follow-up MRI was 228 days. Follow-up MRIs revealed new strokes in 10.6% of patients, cerebral hemorrhages in 4.3%, and no cases of PRES. Additionally, more patients exhibited chronic lacunar infarcts and/or microbleeds, with overall Fazekas scores remaining stable in 66.0%, improving in 31.9%, and worsening in 2.1%. Subgroup analyses based on blood pressure control or follow-up duration showed no significant differences in MRI markers. This study sheds light on the risk of new cerebrovascular events and the dynamic changes in brain MRI markers following acute MHT crisis management. Understanding these changes could lead to improved diagnosis, personalized treatment strategies, and proactive patient care for individuals with MHT.

Transient astrocytic accumulation of fluorescein during spreading depolarizations

Spreading depolarizations (SDs) occur frequently in acute cerebral injuries. They are characterized by a breakdown of transmembrane ion gradients resulting in a reduced extracellular sodium ([Na+]o) and increased extracellular potassium concentration ([K+]o). Elevated [K+]o induces astrocytic swelling, another feature of SD; however, the solutes that drive astrocytic swelling remain incompletely understood. We incidentally found astrocytic accumulation of fluorescein (Fluo) – a low molecular weight anionic dye – during SDs induced by elevated [K+]o. Herein, we aimed to explore the properties of astrocytic Fluo accumulation during SDs, electrical stimulation, [K+]o and glutamate elevation and elucidate underlying mechanisms and its relation to swelling. Experiments were performed in acute neocortical slices from adult male C57Bl6 mice and transgenic mice expressing tdTomato in parvalbumin (PV)-positive neurons. We labeled astrocytes with sulforhodamine-101 (SR-101), measured Fluo kinetics using 2-photon laser scanning microscopy and recorded local field potentials (LFP) to detect SDs. Elevations of [K+]o lead to an increase of the astrocytic Fluo intensity in parallel with astrocytic swelling. Pharmacological inhibitors of sodium‑potassium ATPase (Na/K-ATPase), secondary-active transporters and channels were used to address the underlying mechanisms. Fluo accumulation as well as swelling were only prevented by inhibition of the sodium‑potassium ATPase. Application of glutamate or hypoosmolar solution induced astrocytic swelling independent of Fluo accumulation and glutamate opposed Fluo accumulation when co-administered with high [K+]o. Astrocytes accumulated Fluo and swelled during electrical stimulation and even more during SDs. Taken together, Fluo imaging can be used as a tool to visualize yet unidentified anion fluxes during [K+]o- but not glutamate- or hypoosmolarity induced astrocytic swelling. Fluo imaging may thereby help to elucidate mechanisms of astrocytic swelling and associated fluid movements between brain compartments during physiological and pathological conditions, e.g. SDs.

Early detection of ischemic brain injuries by diffusion-weighted imaging after radiofrequency ablation for fetal reduction in monochorionic pregnancies.

This study aimedto investigate the additional advantages of magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI) over fetal ultrasound in the detection of acute ischemic cerebral injuries in complicated monochorionic (MC) pregnancies that underwent selective reduction by radiofrequency ablation (RFA). This prospective cohort study was conducted on 40 women with complicated MC pregnancies who were treated by RFA. Fetal brain imaging by DWI and conventional MRI was performed either in the early (within 10 days after RFA) or late phase (after 3-6 weeks) in the surviving fetuses to detect both acute and chronic ischemic injuries. The presence of anemia after RFA was also evaluated by Doppler ultrasound. Overall, 13 of the total 43 fetuses (30.23%) demonstrated MRI abnormalities with normal brain ultrasound results including germinal matrix hemorrhage (GMH), extensive cerebral ischemia, and mild ventriculomegaly. Although seven fetuses with GMH eventually survived, fetuses that demonstrated ischemic lesions and ventriculomegaly on MRI died in the uterus. The absence of abnormal cerebral lesions or anemia on ultrasound and Doppler exams does not necessarily rule out fetal brain ischemia. Performing early MRI, particularly DWI seems to be a reasonable option for detection of early intracranial ischemic changes and better management of complicated multiple pregnancies which were treated by RFA.

Depletion of mmu_circ_0001751 (circular RNA Carm1) protects against acute cerebral infarction injuries by binding with microRNA-3098-3p to regulate acyl-CoA synthetase long-chain family member 4

ABSTRACT Circular RNAs (circRNAs) play a critical role in acute cerebral infarction (ACI). Our research discussed the effect of circ-Carm1 in ACI and its potential molecular mechanisms. Healthy controls and patients with ACI were included in this study. The establishment of an oxygen and glucose deprivation/reoxygenation (OGD/R) model of HT22 cells was conducted to mimic ACI in vitro. Quantitative reverse transcription polymerase chain reaction was conducted to determine mRNA levels extracted from serum and HT22 cell samples, and Western blotting was performed to determine protein levels. Terminal deoxynucleotidyl transferase dUTP nick end labeling and cell counting kit 8 assays were conducted to evaluate cellular functions. Concentrations of Fe2+ and malondialdehyde, and levels of transferrin receptor 1, glutathione peroxidase 4, and glutathione were evaluated to determine ferroptosis in OGD/R-induced HT22 cells. The binding relationships between mRNAs and miRNAs were verified. circ-Carm1 was highly expressed in OGD/R-treated HT22 cells. Deficiency of circ-Carm1 restored cell viability and suppressed ferroptosis in OGD/R-induced HT22 cells. miR-3098-3p was predicted to be a target of circ-Carm1. The miR-3098-3p inhibitor partly neutralized the functions of circ-Carm1 in OGD/R-induced HT22 cells. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was confirmed to be a downstream target of miR-3098-3p and was elevated in OGD/R-induced HT22 cells. Overexpression of ACSL4 mitigated the functions of miR-3098-3p and accelerated HT22 cell dysfunction. Hence, circ-Carm1 is upregulated in ACI. circ-Carm1 suppression protects HT22 cells from dysfunction by inhibiting ferroptosis. Therefore, inducing circ-Carm1 deficiency may be a promising therapeutic method for ACI.

Медицинский логопед в мультидисциплинарной реабилитационной команде. Практический опыт Клиники Института Мозга

Background. In domestic and foreign publications, there are no descriptions of the principles of interaction between a medical speech therapist (MST) and other members of a multidisciplinary rehabilitation team (MDRT). Aim. To analyze our own experience in organizing the work of the speech therapy service of the regional neurorehabilitation Center. Materials and methods. We conducted a retrospective analysis of the activities of the division of MST of the interterritorial Center for Neurorehabilitation “Clinic of the Brain Institute“ (CBI) for the period 2015–2019. In the structure of the CBI, there is a 24-hour hospital with 45 beds, including a 9-bed intensive care unit, an 8-bed day hospital, a polyclinic with 50 visits per shift, and a telemedicine center. The speech therapy team of the MDRT consists of 8 specialists with higher education in the specialty “speech pathologist-defectologist“. Speech therapy examination consists of key blocks of clinical diagnosis of speech therapy syndromes: dysphagia, dysarthria, aphasia and prosoparesis. Each block represents a complex of a basic score scale and additional instrumental, including neurophysiological methods. The basis of speech therapy is voice training, articulation and probe massage and other standard procedures, combined in the concept of “basic techniques” for speech therapy syndromes. Drug and non-drug modulations are used to enhance the basic techniques. Results. In the period from 2015 to 2019, 5243 patients were treated in CBI after acute cerebral circulatory disorders and traumatic brain injuries, of which 4273 (81%) needed the help of clinical speech therapists. The most common problem was dysarthria – 55%. Speech breakdown in the framework of aphasia syndrome was noted in 26% of all hospitalized patients. Dysphagia was diagnosed in 30% of all hospitalized patients. During the hospitalization period of 14 days, each patient receives at least 45 minutes of daily individual training with a specialist and group articulation exercises, including weekends. The lesson is preceded by a modulating drug or non-drug procedure. For 5 years, 4273 patients were treated with speech therapy team. In 154 (11.6%) patients, speech therapy syndromes completely regressed, in 28% the severity of their manifestations decreased by 1–2 levels. Conclusion. At the early stage of rehabilitation, the speech therapist is called upon to solve priority tasks: achieving the maximum possible level of independence of the patient, at least staying at home with a minimum level of dependence on the help of a guardian. This is a prerequisite for the implementation of an individual comprehensive rehabilitation program. Despite many methodological and organizational problems, the MST is a key member of the MDRT, without which an effective rehabilitation process is impossible.

EFFICIENCY OF NUTRITIVE SUPPORT IN ACUTE CEREBRAL INJURIES IN THE CONDITIONS OF INTENSIVE THERAPY IN THE AGE ASPECT

Introduction. Metabolic needs vary at different ages. The development of a critical state is changing the need for energy-plastic support. The most energy-dependent organ is the brain, the formation of which in childhood directly depends on the effectiveness of nutritional support. Aim: to evaluate the effectiveness of nutritional support in acute cerebral injuries in infants under intensive care. Materials and methods. Was conducted an observational analytical cohort study of 30 children aged 0 days to 3 months, with the consequences of hypoxic-ischemic encephalopathy (main group) and 20 relatively healthy infants. The delayed gastric evacuation, abdominal bloating, the level of total protein and blood glucose were determined. The results of the study. Abdominal distention was observed in 46.6% of the main group infants, and delayed evacuation of gastric contents was observed in 40% of children (χ2 = 13; p<0.001 and χ2 = 10.5; p<0.001 relative to the comparison group, respectively). In infants of the main group, the indicator of total protein was 58 (38; 62) g / l and was lower relative to the comparison group (p = 0.005). The same changes occurred in the blood glucose level: 3.05 (1.75; 3.7) mmol / l in the main group (p = 0.02). Biochemical parameters correlated with the presence of clinical signs of disorders of the digestive tract. Conclusion. In acute cerebral injuries, there is a development of signs of gastrointestinal insufficiency. These disorders correlate with impaired protein and carbohydrate metabolism and lead to a decrease in total protein and glucose, which indicates a decrease in the effectiveness of nutritional support for patients, including infants.

Multimodal Neuromonitoring and its Impact on Therapeutic and Diagnostic Decisions in Critical Ill Patients

Patients with acute cerebral injuries for various reasons (traumatic, ischemic, hemorrhagic) are at risc for developing secondary brain damage and further neurological deterioration. The aim of neuromonitoring is to recognize subtile changes in intracranial physiology as early as possible to initiate adequate diagnostic and therapeutic measures to prevent secondary brain damage. Beside the classic method of clinical neuromonitoring in awake patients, implantation of intracranial probes to monitor intracranial pressure, brain tissue oxygenation and brain metabolism are used in comatose patients. Electrophysiological monitoring by electrocorticography or evoked potentials and measurement of cerebral blood flow provide additional information.The indications and clinical impact of these various monitoring techniques are discussed to ensure optimal medical care in patients with acute brain injury.

Transplantation of Induced Pluripotent Stem Cells Alleviates Cerebral Inflammation and Neural Damage in Hemorrhagic Stroke.

BackgroundLittle is known about the effects of induced pluripotent stem cell (iPSC) treatment on acute cerebral inflammation and injuries after intracerebral hemorrhage (ICH), though they have shown promising therapeutic potentials in ischemic stoke.MethodsAn ICH model was established by stereotactic injection of collagenase VII into the left striatum of male Sprague-Dawley (SD) rats. Six hours later, ICH rats were randomly divided into two groups and received intracerebrally 10 μl of PBS with or without 1×106 of iPSCs. Subsequently, neural function of all ICH rats was assessed at days 1, 3, 7, 14, 28 and 42 after ICH. Inflammatory cells, cytokines and neural apoptosis in the rats’ perihematomal regions, and brain water content were determined on day 2 or 3 post ICH. iPSC differentiation was determined on day 28 post ICH. Nissl+ cells and glial fibrillary acidic protein (GFAP)+ cells in the perihematoma and the survival rates of rats in two groups were determined on post-ICH day 42.ResultsCompared with control animals, iPSCs treatment not only improved neurological function and survival rate, but also resulted in fewer intracephalic infiltrations of neutrophils and microglia, along with decreased interleukin (IL)-1β, IL-6 and tumour necrosis factor-alpha (TNF-α), and increased IL-10 in the perihematomal tissues of ICH rats. Furthermore, brain oedema formation, apoptosis, injured neurons and glial scar formation were decreased in iPSCs-transplanted rats.ConclusionsOur findings indicate that iPSCs transplantation attenuate cerebral inflammatory reactions and neural injuries after ICH, and suggests that multiple mechanisms including inflammation modulation, neuroprotection and functional recovery might be involved simultaneously in the therapeutic benefit of iPSC treatment against hemorrhagic stroke.

Propofol Impairs Neurogenesis and Neurologic Recovery and Increases Mortality Rate in Adult Rats After Traumatic Brain Injury*

Limited data are available on the influence of sedation for critical care therapy with the widely used anesthetic propofol on recovery from acute traumatic brain injury. To establish the influence of propofol on endogenous neurogenesis and functional recovery after traumatic brain injury, rats were sedated with propofol either during or 2 hours after experimental traumatic brain injury. Randomized controlled animal study. University research laboratory. One hundred sixteen male Sprague Dawley rats. Mechanical brain lesion by controlled cortical impact. This study investigated the dose-dependent influence of propofol (36 or 72 mg/kg/hr) either during controlled cortical impact induction or in a delayed application protocol 2 hours after experimental traumatic brain injury. Infusion of propofol resulted in 1) aggravation of neurologic dysfunction, 2) increased 28-day mortality rate, and 3) impaired posttraumatic neurogenesis (5-bromo-2-deoxyuridine + NeuN-positive cells). Application of propofol during trauma induction afforded a significant stronger effect in the high-dose group compared with low-dose propofol. In the posttrauma protocol, animals were sedated with sevoflurane during the controlled cortical impact injury, and propofol was given after an awake phase. In these animals, propofol increased mortality rate and impaired neurologic function and neurogenesis compared with animals without delayed propofol anesthesia. The results show that propofol may prevent or limit reparative processes in the early-phase postinjury. The results therefore indicate that anesthetics may be potentially harmful not only in very young mammalians but also in adult animals following acute cerebral injuries. The results provide first evidence for an altered sensitivity for anesthesia-related negative effects on neurogenesis, functional outcome, and survival in adult rats with brain lesions.

Lesões cerebrais agudas e sua influência sobre a motilidade gastrintestinal

Subarachnoid hemorrhage can increase intracranial pressure, causing significant morbidity. Acute gastric dilation and delayed gastric emptying are commonly seen in patients with intracranial hypertension, and correction of these gastric abnormalities can facilitate the recovery of patients with brain injuries. We conducted a literature review of both national and international health sciences medical journals and electronic libraries spanning the last twenty-eight years and focused on the brain, gut motility and gastric emptying functional axis either in experimental animal models of brain injury or patients with acute cerebral injuries. Decreased parasympathetic tonus is a potential cause of intracranial hypertension-related food intolerance. Changes in gastrointestinal transit after a brain injury follow a biphasic pattern: an initial phase of accelerated gastric emptying and a late stage of intestinal lethargy. Changes in the physiology underlying gut motility may be essential for homeostatic stabilization in hemodynamically unstable patients. Research studies are necessary to understand the difficult management of intensive care patients with intracranial hypertension secondary to subarachnoid hemorrhages resulting from traumatic brain injuries or rupture of a cerebral aneurysm. Increased intracranial pressure induces massive increases in sympathetic activity, which is responsible for many of the peripheral systemic and gastrointestinal symptoms. Brain injuries leading to significant increases in intracranial pressure result in delayed gastrointestinal emptying due to autonomic nervous system changes.

Neuroanatomical correlates of the clock drawing test in patients with traumatic brain injury

Objective: The clock drawing test (CDT) is a quick and easy to administer test that has traditionally shown parietal lobe dysfunction. The aim of this study was to correlate performance on the CDT with the presence of acute traumatic cerebral injuries sustained after traumatic brain injury (TBI).Methods: A retrospective study was conducted on 170 patients with TBI of all severity admitted to an acute care setting. These patients sustained different types of injuries (epidural haematoma, subdural haematoma, subarachnoid haemorrhage, intraparenchymal haematoma and brain oedema) in different sites (frontal, temporal, parietal, occipital lobes, bilateral and right or left hemisphere).Results: The CDT total score was significantly lower for subjects presenting subarachnoid haemorrhage (4.80 ± 3.34 vs 7.04 ± 3.14, t168df = 4.477, p < 0.001) and for those presenting brain oedema (4.50 ± 3.06 vs 6.69 ± 3.38, t168df = 4.214, p < 0.001), parietal injury (5.15 ± 3.17 vs 6.42 ± 3.52, t168df = 2.416, p = 0.017) or bilateral injuries (5.28 ± 3.31 vs 6.62 ± 3.44, t168df = 2.569, p = 0.011) compared to those who did not.Conclusion: This study provides empirical evidence of the relationship between TBIs and results on the CDT, supporting previous studies done with other populations.

Should Steroids be Offered to Patients With Nonarteritic Anterior Ischemic Optic Neuropathy?

The treatment of nonarteritic anterior optic neuropathy remains very limited and disappointing. Recent publications have suggested that oral steroids as well as intravitreal injections of steroids might be helpful to accelerate resolution of disc edema and improve visual outcome. However, the use of steroids to treat acute NAION remains largely debated.

Decorin suppresses neurocan, brevican, phosphacan and NG2 expression and promotes axon growth across adult rat spinal cord injuries.

The formation of misaligned scar tissue by a variety of cell types expressing multiple axon growth inhibitory proteoglycans presents a physical and molecular barrier to axon regeneration after adult spinal cord injuries. Decorin is a small, leucine-rich proteoglycan that has previously been shown to reduce astrogliosis and basal lamina formation in acute cerebral cortex stab injuries. We have therefore tested whether mini pump infusion of hr-decorin into acute stab injuries of the adult rat spinal cord can not only inhibit formation of an astroglial limitans but also deposition of the axon growth inhibitory proteoglycans neurocan, NG2, phosphacan and brevican. Combined immunohistochemical and quantitative Western blot analysis revealed major reductions in levels of core protein expression (>80% for 130-kDa neurocan, 145/80-kDa brevican, 300-kDa phosphacan) and immunoreactivity for all four chondroitin sulfate proteoglycans (CSPGs) within decorin-treated injuries compared with untreated controls. Astrogliosis within lesion margins and the accumulation of OX42+ macrophages/microglia within lesion centres were also significantly reduced. These decorin-induced changes in scar formation combined to promote the striking ability of axons from microtransplanted adult sensory neurons to enter, grow within and exit decorin-infused spinal cord injuries, in sharp contrast to the complete failure of axons to cross untreated, CSPG-rich lesions. Decorin pretreatment of meningial fibroblasts in vitro also resulted in a three-fold increase in neurite outgrowth from co-cultured adult sensory neurons and suppression of NG2 immunoreactivity. The ability of decorin to promote axon growth across acute spinal cord injuries via a coordinated suppression of inflammation, CSPG expression and astroglial scar formation make decorin treatment a promising component of future spinal cord regeneration strategies.

Status Epilepticus: A Perspective from the Neuroscience Intensive Care Unit

Patients with GCSE and NCSE are common and may present to the emergency department or the NICU. In the NICU, NCSE is a more common presentation than GCSE. In the emergency department, GCSE commonly evolves to NCSE, either as a late sequela of prolonged SE or due to partial treatment with antiepileptic medication or neuromuscular blocking agents. In the emergency department, acute cerebral injuries are commonly found in patients presenting with SE, regardless of whether they have preexisting epilepsy. In the NICU, almost by definition, SE occurs in patients with acute cerebral injuries. Status epilepticus has been found to evolve sequentially through several stages, the end-point of which is a condition of refractory SE leading to neuronal necrosis and permanent cerebral injury. The responsiveness of SE to treatment is time-dependent. This makes early diagnosis and initiation of treatment essential. Most published treatment algorithms stress a 60-minute time window from the diagnosis of SE to its successful control. Unfortunately, the practical problem of patients with SE accessing such treatment protocols has been overlooked. Our preliminary (unpublished) data suggest that this access problem must be solved for treatment algorithms to improve the outcome of SE. In the NICU, access is less of a problem, and the determining factor is early diagnosis by NICU personnel. Because these patients usually sustain NCSE, which can be difficult to diagnose, a high index of suspicion and, optimally, continuous EEG monitoring are necessary for early diagnosis. NICU patients may be more susceptible to the ravages of SE because of their preexisting cerebral injuries. Expedited treatment may therefore be more important in this patient group. Clinical management of SE requires meticulous attention to ventilation and oxygenation, maintenance of adequate blood pressure, prevention of hyperthermia, and close monitoring for cardiac abnormalities. No specific medication is ideal for controlling SE. The knowledgeable and prompt use of intravenous lorazepam, a diazepam-phenytoin combination, or phenobarbital is acceptable as first-line treatment and as part of a systematic treatment algorithm. Refractory SE has been treated conventionally with high-dose intravenous barbiturate coma. Recent evidence suggests that high-dose intravenous midazolam may provide a useful alternative.

ACUTE CEREBRAL INJURIES

During the past decade, since the introduction of methods for cerebral dehydration, the treatment of acute cerebral injuries has become complicated. During this time there has been an increasing tendency in the diagnosis of such lesions for the physiologic reaction of the organism to intracerebral pressure to be superseded by mechanical measurement of intracerebral pressure. Treatment has been guided by the degree of spinal fluid pressure as recorded on the manometer without consideration of the natural defenses of the body or the manifestations that arise when these defenses have reached their limits. Cerebral tissue that is already traumatized has been further insulted by chemical solutions or by intermittent shifts in pressure produced by drainage of the spinal fluid. Finally, the current classifications of these injuries are open to the criticism that they cannot accurately convey the extent of intracerebral damage or aid in most instances in the treatment of the