Improved Neurological Function Research Articles

The impact of refined nursing intervention on neurological function recovery and prognosis improvement in patients undergoing intracranial aneurysm intervention

Background This study aims to explore the application of refined nursing intervention in patients undergoing unruptured intracranial aneurysm intervention, evaluating its impact on neurological function recovery and prognosis improvement. Methods Patients diagnosed with intracranial aneurysms and undergoing treatment at our hospital from February 2022 to June 2023 were included in this study. After applying complete inclusion and exclusion criteria to ensure sample representativeness, a total of 92 patients were enrolled. Using a randomization method, patients were divided into an observation group and a control group. The control group received routine nursing care, while the observation group received refined nursing intervention. Nursing effects were compared between the two groups, and statistical analysis was conducted using appropriate methods, with content analysis summarizing the results. Results The observation group, post-intervention, exhibited significantly improved Neurological Function Deficit (NFD) scores compared to the control group (p = 0.023). Additionally, the observation group showed higher proportions of Grade V patients in the Glasgow Outcome Scale (GOS) post-intervention (p = 0.031). Moreover, Fugl Meyer Assessment (FMA) scores for motor function were notably higher in the observation group than the control group (p = 0.003). The observation group also reported lower headache intensity and fewer adverse outcomes than the control group (p = 0.018, 0.038). Conclusion Refined nursing intervention in patients undergoing intracranial aneurysm intervention demonstrates better outcomes in terms of neurological function recovery and prognosis improvement. It reduces uncertainty in nursing practices, effectively enhancing nursing outcomes, and warrants clinical application and promotion.

Ginsenoside RH1 Improves Neurological Function By Inhibiting Oxidative Stress and Promoting the Expression of Neurotrophic Factors in Cerebral Ischemia-Reperfusion Rats

Ginseng, a valued herb in China, showed efficacies for treatment or prevention of a series of conditions in patients. Ginsenoside Rh1 is the major active component of ginseng. The aim of this study was to investigate the neuroprotective effects of ginsenoside Rh1 on injury of cerebral ischemia-reperfusion in rats. Middle cerebral artery occlusion and reperfusion were performed in male Sprague-Dawley rats. The ischemic stroke rats were treated with ginsenoside Rh1 at dose of 5 mg/kg and 10 mg/kg by gavage. After 7-day treatment, neurological functions of animals were evaluated by adhesive removal tape and beam walking tests. Neuron injury was assessed by immunohistochemical staining. The levels of MDA, BDNF, NGF and activities of SOD, CAT in the ischemic hemisphere were assayed. Treatment with ginsenoside Rh1 for 7 days could significantly improve the neurological functions (P < 0.05)and increase the number of NeuN-positive cells in rats with cerebral ischemia(P < 0.01).Ginsenoside Rh1 decreased significantly MDA level(P < 0.01) and enhanced activitiesof SOD, CAT (P < 0.05 or P < 0.01).Further measurement showed that ginsenoside Rh1 also increased the levels of BDNF, NGF of the ischemic hemisphere(P<0.05 or P<0.01).The present findings demonstrated that ginsenoside Rh1 improved neurological function by inhibiting oxidative stress and promoting the expression of neurotrophic factors after cerebral ischemia-reperfusion.

Pretreatment with Clodronate Improved Neurological Function by Preventing Reduction of Posthemorrhagic Cerebral Blood Flow in Experimental Subarachnoid Hemorrhage.

Brain perivascular macrophages (PVMs) are potential treatment targets for subarachnoid hemorrhage (SAH), and previous studies revealed that their depletion by clodronate (CLD) improved outcomes after experimental SAH. However, the underlying mechanisms are not well understood. Therefore, we investigated whether reducing PVMs by CLD pretreatment improves SAH prognosis by inhibiting posthemorrhagic impairment of cerebral blood flow (CBF). In total, 80 male Sprague-Dawley rats received an intracerebroventricular injection of the vehicle (liposomes) or CLD. Subsequently, the rats were categorized into the prechiasmatic saline injection (sham) and blood injection (SAH) groups after 72h. We assessed its effects on weak and severe SAH, which were induced by 200- and 300-µL arterial blood injections, respectively. In addition, neurological function at 72h and CBF changes from before the intervention to 5min after were assessed in rats after sham/SAH induction as the primary and secondary end points, respectively. CLD significantly reduced PVMs before SAH induction. Although pretreatment with CLD in the weak SAH group provided no additive effects on the primary end point, rats in the severe SAH group showed significant improvement in the rotarod test. In the severe SAH group, CLD inhibited acute reduction of CBF and tended to decrease hypoxia-inducible factor 1α expression. Furthermore, CLD reduced the number of PVMs in rats subjected to sham and SAH surgery, although no effects were observed in oxidative stress and inflammation. Our study proposes that pretreatment with CLD-targeting PVMs can improve the prognosis of severe SAH through a candidate mechanism of inhibition of posthemorrhagic CBF reduction.

Three Days Delayed Recanalization Improved Neurological Function in pMCAO Rats by Increasing M2 Microglia-Possible Involvement of the IL-4R/STAT6/PPARγ Pathway.

Current approved therapies for acute ischemic stroke have a restricted therapeutic time window. Delayed recanalization, which has been utilized clinically in patients who have missed the time window for administration, may be a promising alternative for stroke patients. However, the underlying molecular mechanisms remain undiscovered. Herein, we hypothesized that delayed recanalization would increase M2 microglial polarization through the IL-4R (interleukin-4 receptor)/STAT6 (signal transducer and activators of transcription 6)/PPARγ (peroxisome proliferator-activated receptor γ) pathway, subsequently promoting stroke recovery in rats. The permanent middle cerebral artery occlusion (pMCAO) model was induced via intravascular filament insertion. Recanalization was induced by withdrawing the filament at 3days after MCAO (rMCAO). Interleukin (IL)-4 was administered intranasally at 3days after pMCAO. AS1517499, a specific STAT6 inhibitor, was administered intranasally at 3days after MCAO induction. Immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), western blot analysis, volumetric measurements of brain infarct, and neurological behavior tests were conducted. Delayed recanalization at 3days after MCAO increased the polarization of M2 microglia, decreased inflammation, and improved neurological behavior. IL-4 treatment administered on the 3rd day after pMCAO increased M2 microglial polarization, improved neurological behavior, and reduced infarction volume of pMCAO rats. The inhibition of STAT6 decreased the level of p-STAT6 and PPARγ in rats treated with delayed recanalization. Delayed recanalization improved neurological function by increasing microglial M2 polarization, possibly involved with the IL-4R/STAT6/PPARγ pathway after MCAO in rats.

Triple therapy combined with ventriculoperitoneal shunts can improve neurological function and shorten hospitalization time in non-HIV cryptococcal meningitis patients with increased intracranial pressure

BackgroundRaised intracranial pressure (ICP) and insufficient antifungal regimens are the two main factors result to unsatisfactory outcomes in non-HIV cryptococcal meningitis (CM) patients. In this study, we try to discuss that whether triple therapy of amphotericin B (AmB), fluconazole, 5-flucytosine (5-FC) plus ventriculoperitoneal shunts (VPS) is superior to AmB, 5-FC, fluconazole plus intermittent lumbar puncture in induction therapy in non-HIV CM patients with increased ICP.MethodsWe reviewed 66 clinical records from non-HIV CM patients with increased ICP. The demographic and clinical characteristics, BMRC staging, cerebrospinal fluid profiles (CSF), brain magnetic resonance imaging, treatment, and outcomes of these individuals were retrospectively analyzed. All non-HIV CM patients with increased ICP (≥ 25 cmH2O) were divided into two groups, including 27 patients treated with triple antifungal agents and 39 patients treated with the same triple therapy plus VPS.ResultsTriple therapy plus VPS group had more satisfactory outcomes, more CSF sterilization at 10 weeks follow-up, lower CSF opening pressure, lower BMRC staging scores one week after VPS, less CSF C. neoformans counts and CSF culture positive. Besides, these patients had shorter hospital stay than triple therapy group.ConclusionsTriple antifungal agents combined with VPS could effectively reduce ICP, had faster rate of clearance of C. neoformans counts, more improved neurological function, shorten hospitalization time and better outcomes in non-HIV CM patients with increased ICP. Our study indicated that triple therapy plus early VPS may be an optimal treatment for non-HIV CM patients with increased ICP.

Two Years of Improved Neurological Function With Nusinersen in a 48-Year-Old Patient With Spinal Muscular Atrophy Type 3

Nusinersen antisense oligonucleotide infusions have been shown to be effective in the treatment spinal muscular atrophy. The majority of the evidence has been collected in young type 1 and type 2 patients, and evidence of efficacy in adult patients is limited. A 48-year-old woman with spinal muscular atrophy type 3 who has received the loading dose and 8 maintenance infusions over an 8-month period. Grip and pinch strength, measured by hand-held dynamometry measured at baseline and in 6 to 12 months interval improved over a 24-month period. She also reported multiple other subjective improvements in function. This is the first published case of nusinersen in a middle-aged adult with spinal muscular atrophy. Sustained clinically meaningful improvement may be possible with nusinersen initiation in mid adulthood.

172 - Combinatorial Surgical and Neuroprotective Therapy for Cervical Spondylotic Myelopathy Results in Improved Neurological Function: From Preclinical Proof of Concept to a Phase III Randomized Controlled Trial

172 - Combinatorial Surgical and Neuroprotective Therapy for Cervical Spondylotic Myelopathy Results in Improved Neurological Function: From Preclinical Proof of Concept to a Phase III Randomized Controlled Trial

359 Combinatorial Surgical and Neuroprotective Therapy for Cervical Spondylotic Myelopathy Results in Improved Neurological Function

Abstract INTRODUCTION Surgical decompression is an effective treatment for cervical spondylotic myelopathy (CSM). However, a number of patients continue to experience substantial neurological impairment post surgery. Riluzole has neuroprotective effects in injuries of the central nervous system. To determine the efficacy of riluzole for promoting neurological improvement in CSM following decompression, we performed a pre-clinical proof of concept experiment and then we translated our work and established a Phase III multi-center randomized controlled clinical trial (CSM-Protect). METHODS Surgical decompression was performed in a rat CSM model and riluzole, or control, was administered. Spinal cord blood flow (SCBF) was evaluated in all CSM rats, in vivo, before and after decompression using FAIR MRI. The long-term outcomes of decompression with or without riluzole treatment determined using neurobehavioural and neuroanatomical assessments. Our multi-center double-blind randomized CSM-Protect trial includes a total of 300 CSM patients undergoing decompression surgery and randomized 1:1 to receive riluzole (2 × 50 mg daily for 14 days before and 28 days post surgery) or placebo treatment. MJOA score will determine the effectiveness of the combinatorial treatment at 6 months following surgery. Statistical analysis will be performed as a sequential adaptive trial with interim analysis. RESULTS >Rats receiving combinatorial treatment displayed long-term significant neurological improvements associated with preservation of motor neurons and corticospinal tracts compared to rats treated with decompression alone. Riluzole also dramatically reduced the extent of ischemia-reperfusion injury post surgical decompression in our animal model. At present, 285 subjects have been enrolled into the CSM-Protect trial. A planned interim analysis using this sample has commenced. CONCLUSION The proposed combinatorial therapy promotes neurological recovery in CSM rats. Confirmation of this proof of concept has been translated from bench to the bedside and we are currently running the CSM-Protect trial to determine the efficacy of this combinatorial treatment option for use in CSM patients.

Resveratrol Pretreatment Decreases Ischemic Injury and Improves Neurological Function Via Sonic Hedgehog Signaling After Stroke in Rats.

Resveratrol has neuroprotective effects for ischemic cerebral stroke. However, its neuroprotective mechanism for stroke is less well understood. Beneficial actions of the activated Sonic hedgehog (Shh) signaling pathway in stroke, such as improving neurological function, promoting neurogenesis, anti-oxidative, anti-apoptotic, and pro-angiogenic effects, have been noted, but relatively little is known about the role of Shh signaling in resveratrol-reduced cerebral ischemic injury after stroke. The present study tests whether the Shh pathway mediates resveratrol to decrease cerebral ischemic injury and improve neurological function after stroke. We observed that resveratrol pretreatment significantly improved neurological function, decreased infarct volume, enhanced vitality, and reduced apoptosis of neurons in vivo and vitro after stroke. Meanwhile, expression levels of Shh, Ptc-1, Smo, and Gli-1 mRNAs were significantly upregulated and Gli-1 was relocated to the nucleus. Intriguingly, in vivo and in vitro inhibition of the Shh signaling pathway with cyclopamine, a Smo inhibitor, completely reversed the above effects of resveratrol. These results suggest that decreased cerebral ischemic injury and improved neurological function by resveratrol may be mediated by the Shh signaling pathway.

Inhibition of Phosphatase and Tensin Homolog Deleted on Chromosome 10 Decreases Rat Cortical Neuron Injury and Blood-Brain Barrier Permeability, and Improves Neurological Functional Recovery in Traumatic Brain Injury Model

Background and PurposeRecent evidence has supported the neuroprotective effect of bpV (pic), an inhibitor of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), in models of ischemic stroke. However, whether PTEN inhibitors improve long-term functional recovery after traumatic brain injury (TBI) and whether PTEN affects blood brain barrier (BBB) permeability need further elucidation. The present study was performed to address these issues.MethodsAdult Sprague-Dawley rats were subjected to fluid percussion injury (FPI) after treatment with a well-established PTEN inhibitor bpV (pic) or saline starting 24 h before FPI. Western blotting, real-time quantitative PCR, or immunostaining was used to measure PTEN, p-Akt, or MMP-9 expression. We determined the presence of neuron apoptosis by TUNEL assay. Evans Blue dye extravasation was measured to evaluate the extent of BBB disruption. Functional recovery was assessed by the neurological severity score (NSS), and Kaplan-Meier analysis was used for survival analysis.ResultsPTEN expression was up-regulated after TBI. After bpV (pic) treatment, p-Akt was also up-regulated. We found that bpV (pic) significantly decreased BBB permeability and reduced the number of TUNEL-positive cells. We further demonstrated that PTEN inhibition improved neurological function recovery in the early stage after TBI.ConclusionThese data suggest that treatment with the PTEN inhibitor bpV (pic) has a neuroprotective effect in TBI rats.

A Type-II Positive Allosteric Modulator of α7 nAChRs Reduces Brain Injury and Improves Neurological Function after Focal Cerebral Ischemia in Rats

In the absence of clinically-efficacious therapies for ischemic stroke there is a critical need for development of new therapeutic concepts and approaches for prevention of brain injury secondary to cerebral ischemia. This study tests the hypothesis that administration of PNU-120596, a type-II positive allosteric modulator (PAM-II) of α7 nicotinic acetylcholine receptors (nAChRs), as long as 6 hours after the onset of focal cerebral ischemia significantly reduces brain injury and neurological deficits in an animal model of ischemic stroke. Focal cerebral ischemia was induced by a transient (90 min) middle cerebral artery occlusion (MCAO). Animals were then subdivided into two groups and injected intravenously (i.v.) 6 hours post-MCAO with either 1 mg/kg PNU-120596 (treated group) or vehicle only (untreated group). Measurements of cerebral infarct volumes and neurological behavioral tests were performed 24 hrs post-MCAO. PNU-120596 significantly reduced cerebral infarct volume and improved neurological function as evidenced by the results of Bederson, rolling cylinder and ladder rung walking tests. These results forecast a high therapeutic potential for PAMs-II as effective recruiters and activators of endogenous α7 nAChR-dependent cholinergic pathways to reduce brain injury and improve neurological function after cerebral ischemic stroke.

Multimodal Neuroprotective Therapy With Induced Hypothermia After Ischemic Stroke

Neuroprotective therapies have so far failed to provide improved neurological function and outcome after stroke. A recent focus on multimodal therapies, including the combination of neuroprotective medications with hypothermia, opens a promising new treatment strategy. Advances in hypothermia administration make it one of the most promising neuroprotective therapies available and an ideal candidate for combination with other neuroprotective approaches.

Wnt1 Neuroprotection Translates into Improved Neurological Function during Oxidant Stress and Cerebral Ischemia Through AKT1 and Mitochondrial Apoptotic Pathways

Although essential for the development of the nervous system, Wnt1 also has been associated with neurodegenerative disease and cognitive loss during periods of oxidative stress. Here we show that endogenous expression of Wnt1 is suppressed during oxidative stress in both in vitro and in vivo experimental models. Loss of endogenous Wnt1 signaling directly correlates with neuronal demise and increased functional deficit, illustrating that endogenous neuronal Wnt1 offers a vital level of intrinsic cellular protection against oxidative stress. Furthermore, transient overexpression of Wnt1 or application of exogenous Wnt1 recombinant protein is necessary to preserve neurological function and rescue neurons from apoptotic membrane phosphatidylserine externalization and genomic DNA degradation, since blockade of Wnt1 signaling with a Wnt1 antibody or dickkopf related protein 1 abrogates neuronal protection by Wnt1. Wnt1 ultimately relies upon the activation of Akt1, the modulation of mitochondrial membrane permeability, and the release of cytochrome c to control the apoptotic cascade, since inhibition of Wnt1 signaling, the phosphatidylinositol 3-kinase pathway, or Akt1 activity abrogates the ability of Wnt1 to block these apoptotic components. Our work identifies Wnt1 and its downstream signaling as cellular targets with high clinical potential for novel treatment strategies for multiple disorders precipitated by oxidative stress.