Significant Neurological Impairment Research Articles

Lactobacillus Helveticus Improves Controlled Cortical Impact Injury-Generated Neurological Aberrations by Remodeling of Gut-Brain Axis Mediators.

Considerable studies augured the potential of gut microbiota-based interventions in brain injury-associated complications. Based on our earlier study results, we envisaged the sex-specific neuroprotective effect of Lactobacillus helveticus by remodeling of gut-brain axis. In this study, we investigated the effect of L. helveticus on neurological complications in a mouse model of controlled cortical impact (CCI). Adult, male and female, C57BL/6 mice underwent CCI surgery and received L. helveticus treatment for six weeks. Sensorimotor function was evaluated via neurological severity score and rotarod test. Long-term effects on anxiety-like behavior and cognition were assessed using the elevated-zero maze (EZM) and novel object recognition test (NORT). Brain perilesional area, blood, colon, and fecal samples were collected post-CCI for molecular biology analysis. CCI-operated mice displayed significant neurological impairments at 1-, 3-, 5-, and 7-days post-injury (dpi) and exhibited altered behavior in EZM and NORT compared to sham-operated mice. However, these behavioral changes were ameliorated in mice receiving L. helveticus. GFAP, Iba-1, TNF-α, and IL-1β expressions and corticotrophin-releasing hormone (CRH) levels were elevated in the perilesional cortex of CCI-operated male/female mice. These elevated biomarkers and decreased BDNF levels in both male/female mice were modified by L. helveticus treatment. Additionally, L. helveticus treatment restored altered short-chain fatty acids (SCFAs) levels in fecal samples and improved intestinal integrity but did not affect decreased plasma levels of progesterone and testosterone in CCI mice. These results indicate that L. helveticus exerts beneficial effects in the CCI mouse model by mitigating inflammation and remodeling of gut microbiota-brain mediators.

EOLP-02. END-OF-LIFE CHALLENGES IN NEURO-ONCOLOGICAL PATIENT CARE: A YOUNGNOA SURVEY

Abstract BACKGROUND Malignant brain tumors inevitably relapse, almost always causing significant functional and neurological impairments. Thus, palliative care is crucial in managing individuals with malignant brain tumors. It is essential for neuro-oncologists to be well-prepared to openly communicate about and meet the palliative needs of these patients. With this survey, we sought to evaluate palliative care practices in Germany and their impact on the treatment of neuro-oncological patients. METHODS We conducted an anonymous, interdisciplinary survey targeting palliative care practices among neuro-oncologists in Germany, all members of the Neuro-oncology Working Group of the German Cancer Society. The questionnaire, designed in close coordination with board-certified palliative care specialists, was distributed to 450 physicians. It collected personal information and assessed respondents’ knowledge of and access to palliative care structures. The survey was conducted online from March 31 to April 30, 2023. RESULTS Ninety-two physicians completed the survey. Of these, 81 (88%) reported feeling comfortable with end-of-life conversations, while 11 (12%) did not. No significant differences were observed between the two subgroups regarding their level of medical education (p=0.7140), workplace (p=0.4966), sex (p=0.9999), medical specialty (p=0.5478), or region of practice (p=0.9999). However, those comfortable with end-of-life discussions had significantly more palliative care training either during specialty training (p=0.0475) or through active participation in palliative care courses (p=0.0254). Further detailed analysis is in progress. CONCLUSIONS The survey indicates that while the majority of participants are comfortable with end-of-life discussions, a clear correlation exists between their comfort level and the extent of palliative care training received. This highlights the critical need for enhanced and targeted palliative care education within neuro-oncology training programs to prepare physicians for the complex communication and care challenges in neuro-oncological palliation. Further analysis will continue to explore additional educational and systemic factors that could increase the quality of palliative care in neuro-oncology.

Efficacy of enteral feeding by gastrostomy tube placement in patients with Lennox-Gastaut syndrome on body weight and days of hospitalization: A retrospective case series.

Lennox-Gastaut syndrome (LGS) is a severe form of drug-resistant epilepsy that begins during childhood and frequently leads to significant neurological impairments. Patients with LGS are likely to receive improper oral nutrition because of issues such as dysphagia and aspiration risk, potentially resulting in long-term tube feeding and eventual gastrostomy tube placement. Therefore, we investigated the effects of gastrostomy tube placement on nutrition outcomes and frequency of hospitalization in LGS. We retrospectively examined 67 patients diagnosed with LGS who had undergone gastrostomy tube placement between January 2005 and August 2022. Comprehensive clinical data and complications arising from the procedure were collected. Patients' nutrition condition and frequency of hospitalizations were analyzed before and after gastrostomy tube placement. Gastrostomy tube placement was performed for the following reasons: high risk of aspiration (50 out of 67, 74.6%), dysphagia (13 out of 67, 25.4%), persistent nasogastric tube feeding (2 out of 67, 3.0%), and severe malnutrition (2 out of 67, 3.0%). After the procedure, z scores for weight-for-age improved significantly, shifting from -3.35 ± 3.57 to -2.54 ± 2.70 over a 2-year interval (P < 0.001). Additionally, the total days of hospitalization and days of hospitalization due to respiratory symptoms reduced significantly from 41.94 ± 51.76 to 15.27 ± 26.68 (P < 0.001) and from 23.75 ± 36.92 to 10.52 ± 22.98 (P = 0.009), respectively. Among the patients, 50 (74.6%) experienced complications resulting from gastrostomy, with a relatively small proportion of major complications (11 out of 67, 16.4%) and no mortality. Gastrostomy tube placement is a relatively safe procedure with favorable effects on nutrition status and hospitalization rates in patients with LGS.

German translation and cross-cultural adaptation of the Vestibular Schwannoma Quality of Life Index (VSQOL)

BackgroundVestibular schwannomas (VSs) are benign tumors of the vestibulocochlear nerve that often cause significant neurological and functional impairment. Patient-reported outcomes, including quality of life (QoL), are essential for understanding the overall impact of VS and its treatment. This study aimed to translate and culturally adapt the Vestibular Schwannoma Quality of Life (VSQOL) Index into German to expand its relevance to German-speaking populations.MethodsWe used a qualitative approach including translation and cognitive interviews with 10 patients who underwent VS surgery. The translation process followed the TRAPD protocol to ensure linguistic and conceptual accuracy. Cognitive interviews assessed the comprehensibility and relevance of the translated questionnaire.ResultsThe translation showed remarkable consistency between translators, with minor discrepancies resolved by consensus. Cognitive interviews provided valuable insights that led to refinements in item wording. Participants emphasized the importance of an additional item on physician referrals, reflecting differences in health care systems between the United States and Germany.ConclusionsThe German VSQOL provides a comprehensive tool for assessing QoL in patients with VS that integrates patient-centered dimensions. A Validation study is underway to establish its reliability and validity.

Cavernous Malformations of the Central Nervous System: A Comprehensive Review of Pathophysiology, Diagnosis, and Management.

Cavernous malformations (CMs) of the central nervous system (CNS) are vascular anomalies characterized by clusters of dilated, thin-walled blood vessels prone to leakage and hemorrhage. These malformations can occur throughout the CNS, including the brain and spinal cord, and present with a wide range of clinical manifestations, from asymptomatic cases to severe neurological deficits. Advances in neuroimaging, particularly magnetic resonance imaging (MRI), have greatly improved the diagnosis and understanding of CMs, enabling more precise differentiation from other vascular lesions. The management of CMs has evolved alongside advancements in surgical and radiosurgical techniques, offering various therapeutic options depending on the lesion's characteristics and patient symptoms. While conservative management is often appropriate for asymptomatic or minimally symptomatic lesions, surgical resection or stereotactic radiosurgery may be indicated in cases with recurrent hemorrhage or significant neurological impairment. This comprehensive review explores the pathophysiology, clinical presentation, diagnosis, and management of CMs, highlighting current evidence-based practices and emerging therapeutic approaches. The review also addresses the genetic and molecular underpinnings of CMs, particularly in hereditary cases, and discusses potential future directions in research and treatment. By synthesizing the latest knowledge in the field, this review aims to enhance clinical decision-making and promote further investigation into the optimal management of CMs in the CNS.

Neuroprotective treatment options for neonatal hypoxic-ischemic encephalopathy: Therapeutic hypothermia and beyond

Hypoxic-ischemic encephalopathy (HIE) is the most common form of neonatal encephalopathy that develops due to perinatal asphyxia or ischemia in term and late-preterm infants. It is an important cause of significant neurological impairment and also mortality in newborns worldwide. The pathophysiology of HIE is multifactorial and involves complex cascades of cellular and biochemical events in the brain including excitotoxicity, oxidative stress, inflammation, and cell death, respectively. Therapeutic hypothermia (TH), is the only standard neuroprotective therapy for HIE and is associated with reduced composite outcome of death or major neurodevelopmental disability. However, although TH is beneficial, neonates with HIE still experience unacceptably high rate of devistating morbidities. Therefore, research for adjunctive therapies continue to further improve outcomes in infants with HIE. In this review, both TH and other promising adjunctive neuroprotective therapies are discussed for developing future treatment strategies.

A Comprehensive Review on Current Insights Into Epileptic Encephalopathy: Pathogenesis and Therapeutic Strategies.

Epileptic encephalopathy (EE) represents a challenging group of disorders characterized by severe epilepsy and significant cognitive, behavioral, and neurological impairments. This comprehensive review aims to elucidate the current insights into the pathogenesis and therapeutic strategies for these disorders. Pathogenesis involves a complex interplay of genetic factors, neurobiological mechanisms, and environmental influences that contribute to the severity and progression of symptoms. Clinical manifestations are diverse, encompassing various seizure types, cognitive and behavioral impairments, and developmental delays. Current therapeutic strategies include pharmacological treatments, nonpharmacological interventions, and emerging therapies such as gene and stem cell therapy. Despite advancements, significant challenges and limitations remain, highlighting the need for ongoing research and innovation. This review synthesizes existing knowledge, identifies research gaps, and proposes future directions, emphasizing the potential for personalized medicine to improve patient outcomes and quality of life.

Effect of cannabidiol as a neuroprotective agent on neurodevelopmental impairment in rats with neonatal hypoxia

ObjectiveThis study aims to investigate the neuroprotective effects of cannabidiol (CBD) on neurodevelopmental impairments in rats subjected to neonatal hypoxia, specifically examining its potential to mitigate motor and sensory deficits without the confounding effects of ischemia. MethodsNeonatal Sprague-Dawley rats were allocated to one of four groups: Control, Control-CBD, Hypoxia, and Hypoxia-CBD. Hypoxia was induced on postnatal days 0 and 1. CBD (50 mg/kg) was administered orally for 14 days starting at postnatal day 0. Neurodevelopmental outcomes were assessed using the Neurodevelopmental Reflex Testing in Neonatal Rat Pups scale and the Revised Neurobehavioral Severity Scale for rodents. Statistical analyses were conducted using two-way and one-way ANOVA, with Tukey’s post-hoc tests for group comparisons. ResultsPup weights were recorded on specified postnatal days, with no significant differences observed across the groups (p = 0.1834). Significant neurological impairments due to hypoxia were noted in the Control group compared to the Hypoxia group, particularly in hindlimb grasping on postnatal day 3 (p = 0.0025), posture on postnatal day 12 (p = 0.0073), and in general balance and sound reflex on postnatal day 20 (p = 0.0016 and p = 0.0068, respectively). Additionally, a statistically significant improvement in posture was observed in the Hypoxia-CBD group compared to the Hypoxia group alone (p = 0.0024). ConclusionOur findings indicate that CBD possesses neuroprotective properties that significantly counteract the neurodevelopmental impairments induced by neonatal hypoxia in rats. This study not only supports the therapeutic potential of CBD in managing conditions characterized by neurodevelopmental challenges due to hypoxia but also underscores the necessity for further investigation into the specific molecular mechanisms driving CBD’s neuroprotective effects. Further research is essential to explore CBD’s clinical applications and its potential role in treating human neurodevelopmental disorders.

Toxic-Induced Encephalopathy Following Chemsex in a Young HIV-Positive Male: A Complex Case of Acute Cognitive Impairment with Anterograde Amnesia and Behavioral Alterations.

A broadened clinical spectrum of concomitant complications emerges among the escalating incidence of substance use, particularly within the 'chemsex' context. This case exemplifies the profound neurotoxic repercussions and neurological risk of chemsex in a young HIV-positive male and addresses the multifaceted challenges of such evolving paradigms in substance utilization. After consuming cannabis, poppers, methamphetamine, and cocaine, a 28-year-old HIV-positive male exhibited significant neurological and cognitive impairment. The initial presentation included dysarthria and profound anterograde amnesia. Laboratory findings showed leukocytosis with a PCR of 3mg/dl - elevated cerebrospinal fluid protein levels with no cells. Urine toxicology returned positive for cannabis and amphetamines. A brain CT scan revealed bilateral and symmetrical hippocampi and pale globes hypodensity, indicative of toxic-metabolic encephalopathy. MRI further identified lesions in the globus pallidus, cerebellum, and hippocampi. Following the detection of toxic encephalopathy, Initial neuropsychological was performed screening using the Montreal Cognitive Assessment (MoCA), which highlighted immediate memory deficits. An in-depth neuropsychological assessment conducted 3weeks later included the Wechsler Adult Intelligence Scale-Fourth Edition (WAIS-IV), the Rey Auditory Verbal Learning Test (RAVLT), and tests for visuospatial skills, motor functions, and memory recall. The evaluations revealed pronounced anterograde amnesia, persistent long-term memory inconsistencies, and notable executive function challenges, detailed in Table 1. The detailed analysis of this case underpins the severe neurological consequences that can manifest from heavy substance use. Comprehensive diagnostic evaluations, including neuroimaging and neuropsychological assessments, are crucial in elucidating the full spectrum of substance-induced cognitive impairments. There is an urgent need for enhanced public awareness and preventative measures, especially in the context of chemsex, to bring forth multifaceted health, social, and government implications that modern society must adeptly navigate.

Disease-modifying therapies in managing disability worsening in paediatric-onset multiple sclerosis: a longitudinal analysis of global and national registries

High-efficacy disease-modifying therapies have been proven to slow disability accrual in adults with relapsing-remitting multiple sclerosis. However, their impact on disability worsening in paediatric-onset multiple sclerosis, particularly during the early phases, is not well understood. We evaluated how high-efficacy therapies influence transitions across five disability states, ranging from minimal disability to gait impairment and secondary progressive multiple sclerosis, in people with paediatric-onset multiple sclerosis. Longitudinal data were obtained from the international MSBase registry, containing data from people with multiple sclerosis from 151 centres across 41 countries, and the Italian Multiple Sclerosis and Related Disorders Register, containing data from people with multiple sclerosis from 178 Italian multiple sclerosis centres. People younger than 18 years at the onset of multiple sclerosis symptoms were included, provided they had a confirmed diagnosis of relapsing-remitting multiple sclerosis and at least four Expanded Disability Status Scale (EDSS) scores recorded within 12-month intervals. The primary outcome was the time to change in disability state: minimal disability (EDSS scores 0, 1·0, and 1·5), mild disability (EDSS scores 2·0 and 2·5), moderate disability (EDSS scores 3·0 and 3·5), gait impairment (EDSS scores ≥4·0), and clinician diagnosed secondary progressive multiple sclerosis. A multi-state model was constructed to simulate the natural course of multiple sclerosis, modelling the probabilities of both disability worsening and improvement simultaneously. The impact of high-efficacy disease-modifying therapies (alemtuzumab, cladribine, daclizumab, fingolimod, mitoxantrone, natalizumab, ocrelizumab, rituximab, or autologous haematopoietic stem cell transplantation) and low-efficacy disease-modifying therapies (dimethyl fumarate, glatiramer acetate, interferon beta, or teriflunomide), compared with no treatment, on the course of disability was assessed. Apart from recruitment, individuals with lived experience of multiple sclerosis were not involved in the design and conduct of this study. A total of 5224 people (3686 [70·6%] female and 1538 [29·4%] male) with mean age at onset of multiple sclerosis 15·24 years (SD 2·52) were included. High-efficacy therapies reduced the hazard of disability worsening across the disability states. The largest reduction (hazard ratio 0·41 [95% CI 0·31-0·53]) was observed in participants who were treated with high-efficacy therapies while in the minimal disability state, compared with those remained untreated. The benefit of high-efficacy therapies declined with increasing disability. Young people with minimal disability who received low-efficacy therapy also experienced a reduced hazard (hazard ratio 0·65 [95% CI 0·54-0·77]) of transitioning to mild disability, in contrast to those who remained untreated. Treatment of paediatric-onset relapsing-remitting multiple sclerosis with high-efficacy therapy substantially reduces the risk of reaching key disability milestones. This reduction in risk is most pronounced among young people with minimal or mild disability when treatment began. Children with relapsing-remitting multiple sclerosis should be treated early with high-efficacy therapy, before developing significant neurological impairments, to better preserve their neurological capacity. National Health and Medical Research Council, Australia; MSBase Foundation Fellowship; MS Australia Postdoctoral Fellowship.

Abstract TP318: Evaluating Hypothalamic Injury in a Rat Model of Subarachnoid Hemorrhage

Background and purpose: Hypothalamus is one of the most affected parts of the brain by subarachnoid hemorrhage (SAH). There are some reports that hypothalamic disorders are important determinants of poor prognosis after SAH from acute to chronic phase. However, there have never been any reports on the development of therapeutic strategies targeting the hypothalamus for SAH, and few reports have even demonstrated immunohistological evidence of hypothalamic injury after SAH. Here, we demonstrated on the investigation of temporal changes in hypothalamic injury from the hyperacute phase to the chronic phase after SAH in a rat model of SAH. Methods: Moderate to severe endovascular perforation model of SAH was created using 300g - 450g Sprague-Dawley rats, and they were divided into two groups: Sham operated and SAH group.The endpoints were 3, 6, 12, 24, and 72 hours after SAH, and 7 days and 4 weeks after SAH, and physiological findings and neurological symptoms were measured and hypothalamic injury and related factors in the hypothalamus were studied immunohistochemically. Results: The SAH group showed significant neurological deterioration, and the expression of FJC, indicative of cell death, and TUNEL-positive cells, indicative of apoptosis, in the hypothalamus was significantly elevated in the early phase and decreased over time compared to the sham SAH group. On the other hand, oxytocin, a hypothalamic hormone associated with neuronal protection, was significantly decreased in the SAH group during the acute phase. Conclusions: The present study shows that hypothalamic injury appears hyper acute phase of SAH and persists at least during the acute phase of SAH. These findings suggest that the hypothalamus may be an important therapeutic target in the acute phase of SAH.

Abstract TP319: Time Course of Novel Hypothalamic Protein Sushi Repeat-Containing Protein X- Linked 2 Expression in a Rat Model of Subarachnoid Hemorrhage

Background: Hypothalamic injury after subarachnoid hemorrhage (SAH) is known to be associated with short- and long-term prognosis. Recently, a novel hypothalamic protein, Sushi repeat-containing protein X-linked 2 (SRPX2), was reported as a potential biomarker for hypothalamic damage after traumatic brain injury. However, there are no reports on SRPX2 in SAH, and its role is unknown. In this study, we investigated the expression of SRPX2 in the hypothalamus after SAH using a rat model of SAH. Methods: We made endovascular perforation model of SAH using 300g - 450g SD rats, and they were divided into two groups: Sham operated and SAH group. The endpoints were 3, 6, 12, 24, and 72 hours after SAH, and 7 days and 4 weeks after SAH, and physiological findings and neurological symptoms were measured. In addition, changes in SRPX-2 in the hypothalamic injury and related factors were examined immunohistochemically. Results: The SAH group showed significant neurological deterioration, and a significant decrease in body temperature after 3 h of SAH. Expression of SRPX2 in the hypothalamus was also significantly decreased at 3 h after SAH. However, it was not associated with changes in FJC- and TUNEL-positive cells suggestive of cell death or DHE expression suggestive of oxidative stress. On the other hand, OXT showed a significant decrease after 3 hours of SAH as measured by ELISA in serum from the jugular vein. Conclusions: This is the first study to investigate the expression of SRPX2 in the hypothalamus after SAH time course. Although our results suggest that SRPX2 may not be directly associated with hypothalamic injury after SAH, the fact that SRPX2 expression was decreased during the hyperacute phase and OXT and body temperature were also decreased at the same time suggests that SRPX2 may be indirectly associated with hypothalamic injury after SAH through regulation of endocrine and autonomic function in the hypothalamic-pituitary axis. Further studies are warranted to investigate the possibility that SRPX2 may be indirectly related to hypothalamic disturbances after SAH through endocrine and autonomic regulation of the hypothalamic-pituitary axis.

Pain outcome of non-instrumented lumbar decompressive surgery for degenerative lumbar spine disease using patient-reported pain outcome instruments.

A clinical disorder known as degenerative lumbar spine disease (DLSD) is characterized by persistent low back pain (LBP) coupled with radiculopathy and other signs of neurologic impairment. Using patient-reported pain outcome assessment tools, this study evaluated the pain outcome of non-instrumented lumbar decompressive surgery for DLSD. A prospective longitudinal research was conducted. Using the metric visual analog scale (VAS) score and the Oswestry disability index (ODI), consenting patients who underwent non-instrumented lumbar decompressive surgery for symptomatic DLSD were evaluated for radicular pain and LBP. The evaluation was conducted both immediately before surgery and 6 months after surgery. Data generated by comparing the pre-operative and post-operative VAS and ODI scores were then analyzed using descriptive and inferential statistics. Sixty-seven patients in total completed the study. Thirty-six (54%) males and 31 (46%) females, with a mean age and body mass index of 55.28 years and 29.5 k/m2, respectively. At 6 months postoperatively, there was significant pain reduction from the pre-operative baseline VAS for LBP (67.12-32.74) with P < 0.001, VAS for radicular pain (75.39-32.75) with P < 0.001, and ODI (65.30-27.66) with P < 0.001. There was a greater decrease in radicular pain than in LBP following lumbar decompressive only surgery (P = 0.03). Patients with symptomatic DLSD and high pre-operative back pain scores without considerable listhesis should anticipate a significant reduction in radicular and back pain intensity, as well as pain-related functional disability, 6 months after non-instrumented lumbar decompressive surgery.

SARS-CoV-2 and Brain Health: New Challenges in the Era of the Pandemic.

Respiratory viral infections have been found to have a negative impact on neurological functions, potentially leading to significant neurological impairment. The SARS-CoV-2 virus has precipitated a worldwide pandemic, posing a substantial threat to human lives. Growing evidence suggests that SARS-CoV-2 may severely affect the CNS and respiratory system. The current prevalence of clinical neurological issues associated with SARS-CoV-2 has raised significant concerns. However, there needs to be a more comprehensive understanding of the specific pathways by which SARS-CoV-2 enters the nervous system. Based on the available evidence, this review focuses on the clinical neurological manifestations of SARS-CoV-2 and the possible mechanisms by which SARS-CoV-2 invades the brain.

Vasculitis and Ischemic Stroke in Lyme Neuroborreliosis-Interventional Management Approach and Literature Review.

In rare cases, Lyme neuroborreliosis (LNB) can induce cerebral vasculitis leading to severe stenosis of the cerebral vasculature and consecutive ischemia. Therapy is based on anti-biotic treatment of the tick-borne disease, whereas interventional therapeutic options have not been assessed yet. We report on a patient with LNB and concomitant stenoses and progressive and fatal vasculitis of the cerebral vessels despite all therapeutic efforts by the departments of neurology and interventional neuroradiology. In this context, we also conducted a literature review on endovascular treatment of LNB-associated cerebral ischemia. A 52-year-old female presented with transient neglect and psychomotor slowdown (initial NIHSS = 0). MRI and serology led to the diagnosis of basal meningitis due to LNB with vasculitis of cerebral arteries. Despite immediate treatment with antibiotics and steroids, neurologic deterioration (NIHSS 8) led to an emergency angiography on day 2 after admission. Hemodynamically relevant stenoses of the MCA were treated via spasmolysis and PTA, leading to almost complete neurological recovery. Despite intensified medical treatment, the vasculitis progressed and could only be transiently ameliorated via repetitive spasmolysis. On day 19, she again presented with significant neurologic deterioration (NIHSS 9), and PTA and stenting of the nearly occluded MCA were performed with a patent vessel, initially without hemorrhagic complications. Despite all therapeutic efforts and preserved stent perfusion, vasculitis worsened and the concurrent occurrence of subdural hemorrhage led to the death of the patient. Neuroradiological interventions, i.e., spasmolysis, PTA, and, if necessary, stenting, can and should be considered in cases of LNB-induced vasculitis and stroke that are refractory to best medical treatment alone. Neuroradiological interventions can be considered in patients with vascular complications of Lyme neuroborreliosis as an additional extension of the primary drug therapy.

Unveiling Breakthroughs in Post-resuscitation Supportive Care for Out-of-Hospital Cardiac Arrest Survivors: A Narrative Review.

Survivors of out-of-hospital cardiac arrest (OHCA) experience significant mortality rates and neurological impairment, potentially attributed to the hypoxic-ischemic injury sustained amid the cardiac arrest episode. Post-resuscitation care plays a crucial role in determining outcomes for survivors of OHCA. Supportive therapies have proven to be influential in shaping these outcomes. However, targeting higher blood pressure or oxygen levels during the post-resuscitative phase has not been shown to offer any mortality or neurological benefits. In terms of maintaining hemodynamic instability after resuscitation, it is recommended to use norepinephrine rather than epinephrine. While extracorporeal cardiopulmonary resuscitation has shown promising results, targeted temperature management has been found ineffective in improving outcomes despite its previous potential. This review also investigates various challenges and barriers associated with the practical implementation of these supportive therapies in clinical settings. The review also highlights areas ripe for future research and proposes potential directions to further enhance post-resuscitation supportive care for OHCA survivors.

Case Report on Myleomeningiocele with Cerebellar Tonsillar

Myelomeningocele is a form of neural tube abnormality that causes the spinal cord and meninges to protrude through a hole in the spinal column. It is uncommon for myelomeningocele to be associated with cerebellar tonsillar herniation. This instance demonstrates the difficulties in detecting and controlling this comorbid illness. Myelomeningocele with cerebellar tonsillar herniation is a severe congenital disorder involving the protrusion of the spinal cord and meninges through a defect in the vertebral column, accompanied by downward displacement of the cerebellar tonsils. It is associated with significant neurological and physical impairments, requiring comprehensive medical management and rehabilitation. Early diagnosis, intervention, and on-going multidisciplinary care are crucial for individuals affected by this condition to maximize their potential and improve their overall well-being. We present a case of a female child who was admitted to the NICU for further evaluation and management of myelomeningocele. On examination, the child was active with vitals stable. On local examination, swelling is present at the Lumbosacral region of size 5*4 cm. All investigations and septic screens sent reports within normal limits. MRI was done s/o Spina bifid occulta with LS myelomeningocele with cerebellar tonsillar descent (likely Arnold Chiari Malformation type.

Higher depression scores in cognitively unimpaired individuals affect event‐related potentials similar to those of MCI

AbstractBackgroundDepression is common among seniors, both cognitively unimpaired (CU) and in individuals with Mild Cognitive Impairment (MCI). Electroencephalography (EEG) event‐related Potentials‐P300 is one of the most commonly used electrophysiological parameter associated with cognition. This study aimed to investigate P300 mean amplitude differences between CU individuals and those with MCI, with and without depressive symptoms.MethodThe study included 20 CU individuals with depression [CU‐Dep(+)], 21 MCI patients [MCI‐Dep(+)] with depression, 20 CU individuals without depression [CU‐Dep(‐)] and 22 MCI patients [CU‐Dep(‐)] without depression. Geriatric Depression Scale (GDS) ≥14, was the cut‐off score for classification of Dep (+) or Dep (‐). CU seniors had no significant neurological abnormality or global cognitive impairment. Participants with MCI had cognitive impairment as defined with performances ≥1.5 standard deviations below for age‐and education‐matched controls and with no impairment of daily‐living activities. The ERPs were recorded with a visual classical oddball paradigm, mean P300 amplitudes were measured in the 250‐550ms time window.ResultThe repeated‐measures ANCOVA showed no effect of age and education on P300 but a LOCATION x GROUP interaction [F(6,158) = 2.56,p = 0.035) and main GROUP effect [F(3,79) = 2.56,p = 0.003). Post‐hoc analysis revealed CU‐Dep(‐) had higher P300 amplitudes than MCI‐Dep(+). Moreover, CU‐Dep(+) had lower P300 amplitudes than CU‐Dep(‐) in frontal electrode location. Although there were no significant results, there were a gradual decline trend from CU‐Dep(‐) to MCI‐Dep(+)(Figure 1., Table 2.).ConclusionThe current study showed reduced P300 amplitudes in CU and MCI groups with depression as compared to those without depression. The P300 potential may be a useful tool to determine possible changes or impairments due to sub‐threshold depressive symptoms. However, the lack of significant difference between CU‐Dep(‐) and MCI‐Dep(‐) shows us that the P300 amplitude difference may not always be associated with cognitive status, but may also be associated with depressive symptoms. Thus, it is necessary to consider the depressive symptoms of the participants in cognitive EEG studies.

0992 Reversible Pediatric Central Sleep Apnea in Hyperhomocysteinemia and Cerebral Sinus Venous Thrombosis

Abstract Introduction Pediatric central sleep apnea (CSA) rarely initially presents in adolescent age groups, being more commonly diagnosed in infants. CSA may result from a multitude of neurological insults, such as stroke and brain masses. It may also less often present in metabolic and non-ischemic thrombotic disorders. Report of case(s) A 12-year-old female with history of global developmental delay of unclear etiology, chronic headaches, insulin resistance, and early morning tremors was referred for initial evaluation of possible narcolepsy. Severe daytime sleepiness had acutely worsened over the previous month. She was unable to stay awake during school, despite sleeping 13 hours per 24 hours. Central hypersomnia was suspected and polysomnogram with MSLT was scheduled. The patient presented to the Emergency Department 10 days later for worsening headaches and new oral aversion with 12-pound weight loss. Examination showed ataxic gait and dysarthria. Brain MRI revealed non-occlusive cerebral sinus venous thrombosis (CSVT) involving the superior sagittal sinus, right transverse sinus, right sigmoid sinus, right jugular bulb/vein, and cortical veins overlying both cerebral hemispheres with no stroke. Anticoagulation with enoxaparin was initiated and thrombophilia work-up commenced. Polysomnogram demonstrated a central AHI of 49.9/hr with significant periodic breathing and no obstructive sleep apnea. Oxygen titration sleep study failed to significantly improve CSA and BPAP was initiated. Thrombophilia work-up revealed severe hyperhomocysteinemia. Genetic analysis was consistent with autosomal recessive severe methylenetetrahydrofolate reductase (MTHFR) deficiency. The patient was begun on metabolic treatment with betaine, pyridoxine, hydroxocobalamin, and vitamin C, and transitioned to oral rivaroxaban. At 4 months, blood levels had normalized, and MRI demonstrated resolution of CSVT. Family endorsed BPAP compliance and complete resolution of all sleep symptoms. In addition, there was significant improvement in cognition, interpersonal skills, and abstract thought. Follow up polysomnogram 10 months after presentation demonstrated no CSA nor periodic breathing. Conclusion To our knowledge, this is the first report of MTHFR deficiency and CSVT resulting in severe CSA. While it is difficult to ascertain which entity ultimately caused the CSA, MTHFR deficiency can produce significant neurologic impairment through white matter disease and defective myelination, while CSVT can provoke venous hypertension, venous stasis, or hypoxia. Support (if any)

Intracranial Bleeding in Deep Brain Stimulation Surgery: A Systematic Review and Meta-Analysis

Background: Deep brain stimulation (DBS) is a neurosurgical treatment used for the treatment of movement disorders. Surgical and perioperative complications, although infrequent, can result in clinically significant neurological impairment. Objectives: In this study, we evaluated the incidence and risk factors of intracranial bleeding in DBS surgery. Method: Medline, EMBASE, and Cochrane were screened in line with PRISMA 2020 guidelines to capture studies reporting on the incidence of hemorrhagic events in DBS. After removing duplicates, the search yielded 1,510 papers. s were evaluated by two independent reviewers for relevance. A total of 386 abstracts progressed to the full-text screen and were assessed against eligibility criteria. A total of 151 studies met the criteria and were included in the analysis. Any disagreement between the reviewers was resolved by consensus. Relevant data points were extracted and analyzed in OpenMeta [Analyst] software. Results: The incidence of intracranial bleeding was 2.5% (95% CI: 2.2–2.8%) per each patient and 1.4% (95% CI: 1.2–1.6%) per each implanted lead. There was no statistically significant difference across implantation targets and clinical indications. Patients who developed an intracranial bleed were on average 5 years older (95% CI: 1.26–13.19), but no difference was observed between the genders (p = 0.891). A nonsignificant trend was observed for a higher risk of bleeding in patients with hypertension (OR: 2.99, 95% CI: 0.97–9.19) (p = 0.056). The use of microelectrode recording did not affect the rate of bleeding (p = 0.79). Conclusions: In this review, we find that the rate of bleeding per each implanted lead was 1.4% and that older patients had a higher risk of hemorrhage.