PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Nervous System Diseases - Top 30 Publications

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy-Reply.

Time to Endovascular Thrombectomy for Acute Stroke-Reply.

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy.

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy.

Time to Endovascular Thrombectomy for Acute Stroke.

Medical and Interventional Therapy for Spontaneous Vertebral Artery Dissection in the Craniocervical Segment.

Background and Purpose. Spontaneous vertebral artery dissection (SVAD) is an important reason for posterior-circulation-ischemic stroke in the young and middle-aged population. Although some previous reports reveal a favorable outcome with conservative therapy, it is still controversial in the treatment of SVAD in some specific patients. Herein, we present our 10 years of clinical experience for SVAD at this location. Material and Methods. 20 patients with 20 SVADs in V2 and V3 segments were retrospectively studied. Clinical manifestations and imageology materials were collected and analyzed. All the patients underwent anticoagulation except for one patient because of contraindication. 14 patients underwent Wingspan stents implantation with general anesthesia. Results. In our sample, ischemia (infarction or transient ischemic attack, TIA) was found in all the patients. Angiographic stenosis and dissection aneurysm were the most common findings in the segments mentioned above. 19 of the patients (95%) got the excellent imageological and clinical outcomes. Conclusions. According to our experience in this group, although anticoagulation is effective in vertebral artery dissection, interventional therapy for SVADs in V2 and/or V3 segments is preferred in some specific patients. Stent with higher radial supporting and flexibility, such as Wingspan stent, is suggested.

Biological Basis for Amyloidogenesis in Alzheimer's Disease.

Certain cellular proteins normally soluble in the living organism under certain conditions form aggregates with a specific cross-β sheet structure called amyloid. These intra- or extracellular insoluble aggregates (fibers or plaques) are hallmarks of many neurodegenerative pathologies including Alzheimer's disease (AD), Huntington's disease, Parkinson's disease, prion disease, and other progressive neurological diseases that develop in the aging human central nervous system. Amyloid diseases (amyloidoses) are widespread in the elderly human population, a rapidly expanding demographic in many global populations. Increasing age is the most significant risk factor for neurodegenerative diseases associated with amyloid plaques. To date, nearly three dozen different misfolded proteins targeting brain and other organs have been identified in amyloid diseases and AD, the most prevalent neurodegenerative amyloid disease affecting over 15 million people worldwide. Here we (i) highlight the latest data on mechanisms of amyloid formation and further discuss a hypothesis on the amyloid cascade as a primary mechanism of AD pathogenesis and (ii) review the evolutionary aspects of amyloidosis, which allow new insight on human-specific mechanisms of dementia development.

Molecular Mechanisms Mediating Involvement of Glial Cells in Brain Plastic Remodeling in Epilepsy.

In this review we summarize published data on the involvement of glial cells in molecular mechanisms underlying brain plastic reorganization in epilepsy. The role of astrocytes as glial elements in pathological plasticity in epilepsy is discussed. Data on the involvement of aquaporin-4 in epileptogenic plastic changes and on participation of microglia and extracellular matrix in dysregulation of synaptic transmission and plastic remodeling in epileptic brain tissue are reviewed.

Cooperative Synthesis of Dopamine in Rat Mediobasal Hypothalamus as a Compensatory Mechanism in Hyperprolactinemia.

Dopamine (DA), synthesized in the mediobasal hypothalamus by dopaminergic neurons containing two enzymes of DA synthesis - tyrosine hydroxylase and decarboxylase of aromatic L-amino acids, or by monoenzymatic non-dopaminergic neurons containing one DA synthesis enzyme in cooperation, is known to have an inhibitory effect on prolactin secretion. Deterioration of this inhibitory control leads to an increase in prolactin concentration in the blood and to the development of hyperprolactinemia syndrome. In a rat model of hyperprolactinemia induced by administration of a neurotoxin causing degeneration of dopaminergic and noradrenergic neurons, the level of DA first decreases, leading to an increase in prolactin level (decompensation stage), while later both levels are restored to normal (compensation stage). However, the mechanism of such compensation is still not clear. The aim of the present study was to analyze whether the increase in cooperative synthesis of DA by monoenzymatic neurons during hyperprolactinemia is a manifestation of a compensatory mechanism representing a particular case of neuroplasticity. The level of cooperative synthesis in the hyperprolactinemia model and in the control was estimated as the level of synthesis of DA and L-dihydroxyphenylalanine (L-DOPA) - an intermediate product of DA synthesis, when L-DOPA transfer from neurons containing tyrosine hydroxylase into neurons containing aromatic L-amino acid decarboxylase is inhibited. The level of DA synthesis during the decompensation stage was not changed, while during the compensation stage it was lower than the control. Along with a reduction in DA level, during the compensation stage an increase in the extracellular L-DOPA level in the medium was detected. Thus, the compensation of DA deficiency after degeneration of dopaminergic neurons in the mediobasal hypothalamus is due to the increase in cooperative synthesis of DA by monoenzymatic neurons containing one of the complementary enzymes of the DA synthesis pathway.

Brain Mitochondrial Subproteome of Rpn10-Binding Proteins and Its Changes Induced by the Neurotoxin MPTP and the Neuroprotector Isatin.

Mitochondria play an important role in molecular mechanisms of neuroplasticity, adaptive changes of the brain that occur in the structure and function of its cells in response to altered physiological conditions or development of pathological disorders. Mitochondria are a crucial target for actions of neurotoxins, causing symptoms of Parkinson's disease in various experimental animal models, and also neuroprotectors. Good evidence exists in the literature that mitochondrial dysfunction induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) influences functioning of the ubiquitin-proteasomal system (UPS) responsible for selective proteolytic degradation of proteins from various intracellular compartments (including mitochondria), and neuroprotective effects of certain antiparkinsonian agents (monoamine oxidase inhibitors) may be associated with their effects on UPS. The 19S proteasomal Rpn10 subunit is considered as a ubiquitin receptor responsible for delivery of ubiquitinated proteins to the proteasome proteolytic machinery. In this study, we investigated proteomic profiles of mouse brain mitochondrial Rpn10-binding proteins, brain monoamine oxidase B (MAO B) activity, and their changes induced by a single-dose administration of the neurotoxin MPTP and the neuroprotector isatin. Administration of isatin to mice prevented MPTP-induced inactivation of MAO B and influenced the profile of brain mitochondrial Rpn10-binding proteins, in which two pools of proteins were clearly recognized. The constitutive pool was insensitive to neurotoxic/neuroprotective treatments, while the variable pool was specifically influenced by MPTP and the neuroprotector isatin. Taking into consideration that the neuroprotective dose of isatin used in this study can result in brain isatin concentrations that are proapoptotic for cells in vitro, the altered repertoire of mitochondrial Rpn10-binding proteins may thus represent a part of a switch mechanism from targeted elimination of individual (damaged) proteins to more efficient ("global") elimination of damaged organelles and whole damaged cells.

Impact of Changes in Neurotrophic Supplementation on Development of Alzheimer's Disease-Like Pathology in Oxys Rats.

Alzheimer's disease (AD) is the most common type of age-related dementia. The development of neurodegeneration in AD is closely related to alterations in neurotrophic supplementation of the brain, which may be caused either by disorder of neurotrophin metabolism or by modification of its availability due to changes in the microenvironment of neurons. The underlying mechanisms are not fully understood. In this work, we used senescence-accelerated OXYS rats as a unique model of the sporadic form of AD to examine the relationship of development of AD signs and changes in neurotrophic supplementation of the cortex. Based on comparative analysis of the transcriptome of the frontal cerebral cortex of OXYS and Wistar (control) rats, genes of a neurotrophin signaling pathway with different mRNA levels in the period prior to the development of AD-like pathology in OXYS rats (20 days) and in the period of its active manifestation (5 months) and progression (18 months) were identified. The most significant changes in mRNA levels in the cortex of OXYS rats occurred in the period from 5 to 18 months of age. These genes were associated with neurogenesis, neuronal differentiation, synaptic plasticity, and immune response. The results were compared to changes in the levels of brain-derived neurotrophic factor (BDNF), its receptors TrkB and p75(NTR), as well as with patterns of their colocalization, which reveal the balance of proneurotrophins and mature neurotrophins and their receptors. We found that alterations in neurotrophic balance indicating increased apoptosis precede the development of AD-like pathology in OXYS rats. Manifestation of AD-like pathology occurs against a background of activation of compensatory and regenerative processes including increased neurotrophic supplementation. Active progression of AD-like pathology in OXYS rats is accompanied by the suppression of activity of the neurotrophin system. Thus, the results confirm the importance of the neurotrophin system as a potential target for development of new approaches to slow age-related alterations in brain and AD development.

Status Epilepticus Impairs Synaptic Plasticity in Rat Hippocampus and Is Followed by Changes in Expression of NMDA Receptors.

Cognitive deficits and memory loss are frequent in patients with temporal lobe epilepsy. Persistent changes in synaptic efficacy are considered as a cellular substrate underlying memory processes. Electrophysiological studies have shown that the properties of short-term and long-term synaptic plasticity in the cortex and hippocampus may undergo substantial changes after seizures. However, the neural mechanisms responsible for these changes are not clear. In this study, we investigated the properties of short-term and long-term synaptic plasticity in rat hippocampal slices 24 h after pentylenetetrazole (PTZ)-induced status epilepticus. We found that the induction of long-term potentiation (LTP) in CA1 pyramidal cells is reduced compared to the control, while short-term facilitation is increased. The experimental results do not support the hypothesis that status epilepticus leads to background potentiation of hippocampal synapses and further LTP induction becomes weaker due to occlusion, as the dependence of synaptic responses on the strength of input stimulation was not different in the control and experimental animals. The decrease in LTP can be caused by impairment of molecular mechanisms of neuronal plasticity, including those associated with NMDA receptors and/or changes in their subunit composition. Real-time PCR demonstrated significant increases in the expression of GluN1 and GluN2A subunits 3 h after PTZ-induced status epilepticus. The overexpression of obligate GluN1 subunit suggests an increase in the total number of NMDA receptors in the hippocampus. A 3-fold increase in the expression of the GluN2B subunit observed 24 h after PTZ-induced status epilepticus might be indicative of an increase in the proportion of GluN2B-containing NMDA receptors. Increased expression of the GluN2B subunit may be a cause for reducing the magnitude of LTP at hippocampal synapses after status epilepticus.

Clinical outcome and molecular characterization of brain metastases from esophageal and gastric cancer: a systematic review.

The aim of the study was to collect the available data on central nervous system (CNS) metastases from esophageal and gastric cancer. A PubMed, EMBASE, SCOPUS, Web of Science, LILACS, Ovid and Cochrane Library search was performed. Thirty-seven studies including 779 patients were considered. Among the data extracted, treatment of tumor and brain metastases (BMs), time to BMs development, number and subsite, extracerebral metastases rate, median overall survival (OS) and prognostic factors were included. For esophageal cancer, the median OS from diagnosis of BMs was 4.2 months. Prognostic factors for OS included: performance status, multimodal therapy, adjuvant chemotherapy, single BM, brain only disease and surgery. For gastric cancer, median OS was 2.4 months. Prognostic factors for OS included: recursive partitioning analysis class 2, stereotactic radiosurgery (SRT) and use of intrathecal therapy. HER2-positive gastric cancer was shown to be associated with a higher risk and shorter time to CNS relapse. Patients harboring BMs from gastric and esophageal tumors, except cases with single lesions that are treated aggressively, have a poor prognosis. SRT (plus or minus surgery and whole brain radiotherapy) seems to give better results in terms of longer OS after brain relapse.

Primary central nervous system lymphoma: essential points in diagnosis and management.

Primary central nervous system lymphoma (PCNSL) is an extra-nodal non-Hodgkin lymphoma. PCNSL is defined as lymphoma involving the brain, leptomeninges, eyes, or spinal cord without evidence of lymphoma outside the CNS. Treatment includes induction with chemotherapy and consolidation with whole-brain radiotherapy or high-dose chemotherapy supported by autologous stem cell transplantation. High-dose methotrexate is the most important drug in cases with PCNSL, and this drug will be used in combination with small molecules, BTK inhibitors, new monoclonal antibodies, and checkpoint blockers.

Hypothermia for Convulsive Status Epilepticus.

Hypothermia for Convulsive Status Epilepticus.

Hypothermia for Convulsive Status Epilepticus.

Case Report of Serratus Plane Catheter for Pain Management in a Patient With Multiple Rib Fractures and an Inferior Scapular Fracture.

We placed a superficial serratus anterior plane catheter in an elderly woman with dementia and elevated clotting times who presented with multiple rib fractures after a mechanical fall. She was not a surgical candidate, and treatment consisted of conservative management with physical therapy and pain control. She was not a candidate for a patient-controlled analgesia regimen because of her dementia. Given her elevated international normalized ratio, thoracic epidural and paravertebral analgesia was also contraindicated. We placed an ultrasound-guided serratus anterior plane catheter, allowing titratable continuous infusion in a trauma patient, resulting in excellent analgesia without adverse effects.

Syncope: Evaluation and Differential Diagnosis.

Syncope is an abrupt and transient loss of consciousness caused by cerebral hypoperfusion. It accounts for 1% to 1.5% of emergency department visits, resulting in high hospital admission rates and significant medical costs. Syncope is classified as neurally mediated, cardiac, and orthostatic hypotension. Neurally mediated syncope is the most common type and has a benign course, whereas cardiac syncope is associated with increased morbidity and mortality. Patients with presyncope have similar prognoses to those with syncope and should undergo a similar evaluation. A standardized approach to syncope evaluation reduces hospital admissions and medical costs, and increases diagnostic accuracy. The initial assessment for all patients presenting with syncope includes a detailed history, physical examination, and electrocardiography. The initial evaluation may diagnose up to 50% of patients and allows immediate short-term risk stratification. Laboratory testing and neuroimaging have a low diagnostic yield and should be ordered only if clinically indicated. Several comparable clinical decision rules can be used to assess the short-term risk of death and the need for hospital admission. Low-risk patients with a single episode of syncope can often be reassured with no further investigation. High-risk patients with cardiovascular or structural heart disease, history concerning for arrhythmia, abnormal electrocardiographic findings, or severe comorbidities should be admitted to the hospital for further evaluation. In cases of unexplained syncope, provocative testing and prolonged electrocardiographic monitoring strategies can be diagnostic. The treatment of neurally mediated and orthostatic hypotension syncope is largely supportive, although severe cases may require pharmacotherapy. Cardiac syncope may require cardiac device placement or ablation.

Anterior condylar confluence dural arteriovenous fistula: a rare cause of hoarseness.

Hoarseness secondary to an anterior condylar confluence (ACC) dural arteriovenous fistula (DAVF) has not been previously described. We present a 58-year-old patient with a 3-week history of progressive unilateral left-sided headaches and hoarseness. Nasolaryngoscopy and CT neck showed the presence of unilateral vocal cord palsy with no identifiable cause along the expected course of the recurrent laryngeal nerve. MRI revealed an incidental finding of abnormal serpiginous vessels in the left hypoglossal canal which led to a diagnostic cerebral angiogram, confirming the presence of an ACC DAVF. The patient underwent transvenous coil embolisation with subsequent resolution of arteriovenous shunting and symptoms. Follow-up MRI at 6 months showed no recurrence and there was complete resolution of clinical symptoms.

Carotid artery dissection: a rare complication of Eagle syndrome.

Carotid artery dissection is a significant cause of ischaemic stroke in all age groups and accounts for a large percentage of strokes in young patients. Carotid dissection can be caused by trauma, underlying connective tissue disease, hypertension, mechanical injury or can be spontaneous. We present an exceedingly rare case of carotid dissection caused by an elongated styloid process, causing direct mechanical damage to the carotid artery.

Immunological diagnosis as an adjunctive tool for an early diagnosis of tuberculous meningitis of an immune competent child in a low tuberculosis endemic country: a case report.

Pediatric tuberculous meningitis is a highly morbid, often fatal disease. Its prompt diagnosis and treatment saves lives, in fact delays in the initiation of therapy have been associated with high mortality rates.

Spinal arachnoid cysts - our experience and review of literature.

Arachnoid cysts are discrete pockets of CSF or CSF-like fluid found adjacent to normal CSF spaces, either spinal or cranial. Spinal arachnoid cysts (SAC) are most commonly extradural, however intradural or perineural are also described.

A Precision Medicine Initiative for Alzheimer's disease: the road ahead to biomarker-guided integrative disease modeling.

After intense scientific exploration and more than a decade of failed trials, Alzheimer's disease (AD) remains a fatal global epidemic. A traditional research and drug development paradigm continues to target heterogeneous late-stage clinically phenotyped patients with single 'magic bullet' drugs. Here, we propose that it is time for a paradigm shift towards the implementation of precision medicine (PM) for enhanced risk screening, detection, treatment, and prevention of AD. The overarching structure of how PM for AD can be achieved will be provided through the convergence of breakthrough technological advances, including big data science, systems biology, genomic sequencing, blood-based biomarkers, integrated disease modeling and P4 medicine. It is hypothesized that deconstructing AD into multiple genetic and biological subsets existing within this heterogeneous target population will provide an effective PM strategy for treating individual patients with the specific agent(s) that are likely to work best based on the specific individual biological make-up. The Alzheimer's Precision Medicine Initiative (APMI) is an international collaboration of leading interdisciplinary clinicians and scientists devoted towards the implementation of PM in Neurology, Psychiatry and Neuroscience. It is hypothesized that successful realization of PM in AD and other neurodegenerative diseases will result in breakthrough therapies, such as in oncology, with optimized safety profiles, better responder rates and treatment responses, particularly through biomarker-guided early preclinical disease-stage clinical trials.

The Efficacy of Acupuncture for Treating Depression-Related Insomnia Compared with a Control Group: A Systematic Review and Meta-Analysis.

Objective. To evaluate the effectiveness of acupuncture as monotherapy and as an alternative therapy in treating depression-related insomnia. Data Source. Seven databases were searched starting from 1946 to March 30, 2016. Study Eligibility Criteria. Randomized-controlled trials of adult subjects (18-75 y) who had depression-related insomnia and had received acupuncture. Results. 18 randomized-controlled clinical trials (RCTs) were introduced in this meta-analysis. The findings determined that the acupuncture treatment made significant improvements in PSQI score (MD = -2.37, 95% CI -3.52 to -1.21) compared with Western medicine. Acupuncture combined with Western medicine had a better effect on improving sleep quality (MD = -2.63, 95% CI -4.40 to -0.86) compared with the treatment of Western medicine alone. There was no statistical difference (MD = -2.76, 95% CI -7.65 to 2.12) between acupuncture treatment and Western medicine towards improving the HAMD score. Acupuncture combined with Western medicine (MD = -5.46, CI -8.55 to -2.38) had more effect on improving depression degree compared with the Western medicine alone. Conclusion. This systematic review indicates that acupuncture could be an alternative therapy to medication for treating depression-related insomnia.

Orthostatic Intolerance and Postural Orthostatic Tachycardia Syndrome in Joint Hypermobility Syndrome/Ehlers-Danlos Syndrome, Hypermobility Type: Neurovegetative Dysregulation or Autonomic Failure?

Background. Joint hypermobility syndrome/Ehlers-Danlos syndrome, hypermobility type (JHS/EDS-HT), is a hereditary connective tissue disorder mainly characterized by generalized joint hypermobility, skin texture abnormalities, and visceral and vascular dysfunctions, also comprising symptoms of autonomic dysfunction. This study aims to further evaluate cardiovascular autonomic involvement in JHS/EDS-HT by a battery of functional tests. Methods. The response to cardiovascular reflex tests comprising deep breathing, Valsalva maneuver, 30/15 ratio, handgrip test, and head-up tilt test was studied in 35 JHS/EDS-HT adults. Heart rate and blood pressure variability was also investigated by spectral analysis in comparison to age and sex healthy matched group. Results. Valsalva ratio was normal in all patients, but 37.2% of them were not able to finish the test. At tilt, 48.6% patients showed postural orthostatic tachycardia, 31.4% orthostatic intolerance, 20% normal results. Only one patient had orthostatic hypotension. Spectral analysis showed significant higher baroreflex sensitivity values at rest compared to controls. Conclusions. This study confirms the abnormal cardiovascular autonomic profile in adults with JHS/EDS-HT and found the higher baroreflex sensitivity as a potential disease marker and clue for future research.

Effects of Wrist Posture and Fingertip Force on Median Nerve Blood Flow Velocity.

Purpose. The purpose of this study was to assess nerve hypervascularization using high resolution ultrasonography to determine the effects of wrist posture and fingertip force on median nerve blood flow at the wrist in healthy participants and those experiencing carpal tunnel syndrome (CTS) symptoms. Methods. The median nerves of nine healthy participants and nine participants experiencing symptoms of CTS were evaluated using optimized ultrasonography in five wrist postures with and without a middle digit fingertip press (0, 6 N). Results. Both wrist posture and fingertip force had significant main effects on mean peak blood flow velocity. Blood flow velocity with a neutral wrist (2.87 cm/s) was significantly lower than flexed 30° (3.37 cm/s), flexed 15° (3.27 cm/s), and extended 30° (3.29 cm/s). Similarly, median nerve blood flow velocity was lower without force (2.81 cm/s) than with force (3.56 cm/s). A significant difference was not found between groups. Discussion. Vascular changes associated with CTS may be acutely induced by nonneutral wrist postures and fingertip force. This study represents an early evaluation of intraneural blood flow as a measure of nerve hypervascularization in response to occupational risk factors and advances our understanding of the vascular phenomena associated with peripheral nerve compression.

Phase I and Phase II Therapies for Acute Ischemic Stroke: An Update on Currently Studied Drugs in Clinical Research.

Acute ischemic stroke is a devastating cause of death and disability, consequences of which depend on the time from ischemia onset to treatment, the affected brain region, and its size. The main targets of ischemic stroke therapy aim to restore tissue perfusion in the ischemic penumbra in order to decrease the total infarct area by maintaining blood flow. Advances in research of pathological process and pathways during acute ischemia have resulted in improvement of new treatment strategies apart from restoring perfusion. Additionally, limiting the injury severity by manipulating the molecular mechanisms during ischemia has become a promising approach, especially in animal research. The purpose of this article is to review completed and ongoing phases I and II trials for the treatment of acute ischemic stroke, reviewing studies on antithrombotic, thrombolytic, neuroprotective, and antineuroinflammatory drugs that may translate into more effective treatments.

Unilateral malignant optic glioma following glioblastoma multiforme in the young: a case report and literature review.

Malignant optic gliomas are rare, but they rapidly become lethal visual pathway tumors. We present the clinical course, treatment, and prognosis of a case of unilateral malignant optic glioma in a young man with a history of brain glioblastoma multiforme (GBM).

Behavioral Treatments for Post-Traumatic Headache.

Post-traumatic headache (PTH) is a common headache type after traumatic brain injury (TBI). There are no FDA approved medications for PTH, and it is unknown how medications can affect the brain's ability to recover from TBI. Thus, we sought to examine the biopsychosocial factors that influence PTH and the non-pharmacologic treatments studied for headache treatment. We also sought to determine if there is literature examining whether the non-pharmacologic treatments influence the biopsychosocial factors. The non-pharmacologic treatments assessed included cognitive behavioral therapy (CBT), biofeedback, progressive muscle relaxation therapy (PMR), acupuncture, and physical therapy (PT).