Brain Maps May Reveal the Origins and Paths of Neurological Dysfunction

Abstract Background and Study Aim Cervical spondylotic myelopathy (CSM) is a common degenerative disease that mainly occurs in elder patients, leading to different degrees of neurological dysfunction. Spinal cord involvement is mainly distributed at the C3–C7 segments, but it may also involve up to the C2 level. This study aimed to assess the clinical efficacy and safety of open-door laminoplasty using a new extensor attachment-point reconstruction technique for treating CSM involving the C2 segment. Patients and Methods Fifty-nine patients with CSM involving the C2 segment and undergoing open-door laminoplasty were included in this retrospective study. Based on the titanium plate used in the operation, patients were divided into two groups, a reconstructed titanium plate fixation (RPF) group (n = 28) and a conventional titanium plate fixation (CPF) group (n = 31). Improvements in neurological function, cervical range of motion (ROM), cervical curvature index (CCI), preservation of posterior cervical muscle mass, and axial symptoms were compared between the two groups. Results There were no significant differences in operative time and intraoperative blood loss between the groups (p > 0.05). The Japanese Orthopaedic Association (JOA) score significantly increased in both groups postsurgery (p < 0.05); the neurological recovery rate was similar between the two groups (64.1 ± 13.3% vs. 65.9 ± 14.7%, p > 0.05). There was no significant loss of cervical ROM in either group (p > 0.05). The anteroposterior dural sac diameter at the C2 level was significantly enlarged in both groups (p < 0.05). Alternatively, CCI was significantly reduced in the CRP group (p < 0.05) but unchanged in the RPF group (p > 0.05). The cross-sectional area of the posterior cervical muscles was also significantly reduced in the CPF group (p < 0.05) but maintained in the RPF group (p > 0.05). Finally, axial symptoms were more severe in the CPF group than in the RPF group (p < 0.05). Conclusion Laminoplasty is an effective surgical procedure for CSM involving the C2 segment. The reconstructed titanium plate achieved superior maintenance of cervical curvature and reduced both muscle atrophy and severity of axial symptoms compared with titanium conventional plates.

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Neurological Evaluation of Patients with Newly Diagnosed Coeliac Disease Presenting to Gastroenterologists: A 7-Year Follow-Up Study

Nutrients ◽

10.3390/nu13061846 ◽

2021 ◽

Vol 13 (6) ◽

pp. 1846

Author(s):

Marios Hadjivassiliou ◽

Iain D. Croall ◽

Richard A. Grünewald ◽

Nick Trott ◽

David S. Sanders ◽

...

Keyword(s):

Coeliac Disease ◽

Brain Imaging ◽

Cerebellar Atrophy ◽

Neurological Dysfunction ◽

Close Monitoring ◽

Newly Diagnosed ◽

Positive Serology ◽

Original Cohort ◽

Follow Up Study

We have previously shown that 67% of patients with newly diagnosed coeliac disease (CD) presenting to gastroenterologists have evidence of neurological dysfunction. This manifested with headache and loss of co-ordination. Furthermore 60% of these patients had abnormal brain imaging. In this follow-up study, we re-examined and re-scanned 30 patients from the original cohort of 100, seven years later. There was significant reduction in the prevalence of headaches (47% to 20%) but an increase in the prevalence of incoordination (27% to 47%). Although those patients with coordination problems at baseline reported improvement on the gluten free diet (GFD), there were 7 patients reporting incoordination not present at baseline. All 7 patients had positive serology for one or more gluten-sensitivity related antibodies at follow-up. In total, 50% of the whole follow-up cohort were positive for one or more gluten-related antibodies. A comparison between the baseline and follow-up brain imaging showed a greater rate of cerebellar grey matter atrophy in the antibody positive group compared to the antibody negative group. Patients with CD who do not adhere to a strict GFD and are serological positive are at risk of developing ataxia, and have a significantly higher rate of cerebellar atrophy when compared to patients with negative serology. This highlights the importance of regular review and close monitoring.

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Targeting the Cerebrovascular System: Next-Generation Biomarkers and Treatment for Mild Traumatic Brain Injury

The Neuroscientist ◽

10.1177/10738584211012264 ◽

2021 ◽

pp. 107385842110122

Author(s):

Tamara L. Baker ◽

Denes V. Agoston ◽

Rhys D. Brady ◽

Brendan Major ◽

Stuart J. McDonald ◽

...

Keyword(s):

Brain Function ◽

Brain Injuries ◽

Neurological Dysfunction ◽

Clinical Approach ◽

Cerebral Vasculature ◽

Review Of The Literature ◽

Cerebrovascular Injury ◽

Medical Issues ◽

And Function ◽

Cerebrovascular System

The diagnosis, prognosis, and treatment of mild traumatic brain injuries (mTBIs), such as concussions, are significant unmet medical issues. The kinetic forces that occur in mTBI adversely affect the cerebral vasculature, making cerebrovascular injury (CVI) a pathophysiological hallmark of mTBI. Given the importance of a healthy cerebrovascular system in overall brain function, CVI is likely to contribute to neurological dysfunction after mTBI. As such, CVI and related pathomechanisms may provide objective biomarkers and therapeutic targets to improve the clinical management and outcomes of mTBI. Despite this potential, until recently, few studies have focused on the cerebral vasculature in this context. This article will begin by providing a brief overview of the cerebrovascular system followed by a review of the literature regarding how mTBI can affect the integrity and function of the cerebrovascular system, and how this may ultimately contribute to neurological dysfunction and neurodegenerative conditions. We then discuss promising avenues of research related to mTBI biomarkers and interventions that target CVI, and conclude that a clinical approach that takes CVI into account could result in substantial improvements in the care and outcomes of patients with mTBI.

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Predictive Value of Subacute Heart Rate Variability for Determining Outcome Following Adolescent Concussion

Journal of Clinical Medicine ◽

10.3390/jcm10010161 ◽

2021 ◽

Vol 10 (1) ◽

pp. 161

Author(s):

Colt A. Coffman ◽

Jacob J. M. Kay ◽

Kat M. Saba ◽

Adam T. Harrison ◽

Jeffrey P. Holloway ◽

...

Keyword(s):

Heart Rate ◽

Heart Rate Variability ◽

Cognitive Performance ◽

Predictive Value ◽

System Integration ◽

Sports Medicine ◽

Clinical Symptoms ◽

Physiological Stress ◽

Neurological Dysfunction ◽

Neurobehavioral Function

Objective assessments of concussion recovery are crucial for facilitating effective clinical management. However, predictive tools for determining adolescent concussion outcomes are currently limited. Research suggests that heart rate variability (HRV) represents an indirect and objective marker of central and peripheral nervous system integration. Therefore, it may effectively identify underlying deficits and reliably predict the symptomology following concussion. Thus, the present study sought to evaluate the relationship between HRV and adolescent concussion outcomes. Furthermore, we sought to examine its predictive value for assessing outcomes. Fifty-five concussed adolescents (12–17 years old) recruited from a local sports medicine clinic were assessed during the initial subacute evaluation (within 15 days postinjury) and instructed to follow up for a post-acute evaluation. Self-reported clinical and depressive symptoms, neurobehavioral function, and cognitive performance were collected at each timepoint. Short-term HRV metrics via photoplethysmography were obtained under resting conditions and physiological stress. Regression analyses demonstrated significant associations between HRV metrics, clinical symptoms, neurobehavioral function, and cognitive performance at the subacute evaluation. Importantly, the analyses illustrated that subacute HRV metrics significantly predicted diminished post-acute neurobehavioral function and cognitive performance. These findings indicate that subacute HRV metrics may serve as a viable predictive biomarker for identifying underlying neurological dysfunction following concussion and predict late cognitive outcomes.

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Cognitive impairments induced by necrotizing enterocolitis can be prevented by inhibiting microglial activation in mouse brain

Science Translational Medicine ◽

10.1126/scitranslmed.aan0237 ◽

2018 ◽

Vol 10 (471) ◽

pp. eaan0237 ◽

Cited By ~ 29

Author(s):

Diego F. Niño ◽

Qinjie Zhou ◽

Yukihiro Yamaguchi ◽

Laura Y. Martin ◽

Sanxia Wang ◽

...

Keyword(s):

Necrotizing Enterocolitis ◽

Microglial Activation ◽

Gastrointestinal Disease ◽

Cognitive Impairments ◽

High Mobility ◽

Neurological Dysfunction ◽

Mucosal Inflammation ◽

Signaling Axis ◽

The Brain

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant. One of the most important long-term complications observed in children who survive NEC early in life is the development of profound neurological impairments. However, the pathways leading to NEC-associated neurological impairments remain unknown, thus limiting the development of prevention strategies. We have recently shown that NEC development is dependent on the expression of the lipopolysaccharide receptor Toll-like receptor 4 (TLR4) on the intestinal epithelium, whose activation by bacteria in the newborn gut leads to mucosal inflammation. Here, we hypothesized that damage-induced production of TLR4 endogenous ligands in the intestine might lead to activation of microglial cells in the brain and promote cognitive impairments. We identified a gut-brain signaling axis in an NEC mouse model in which activation of intestinal TLR4 signaling led to release of high-mobility group box 1 in the intestine that, in turn, promoted microglial activation in the brain and neurological dysfunction. We further demonstrated that an orally administered dendrimer-based nanotherapeutic approach to targeting activated microglia could prevent NEC-associated neurological dysfunction in neonatal mice. These findings shed light on the molecular pathways leading to the development of NEC-associated brain injury, provide a rationale for early removal of diseased intestine in NEC, and indicate the potential of targeted therapies that protect the developing brain in the treatment of NEC in early childhood.

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Differential role of SIRT1/MAPK pathway during cerebral ischemia in rats and humans

Scientific Reports ◽

10.1038/s41598-021-85577-9 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Sireesh Kumar Teertam ◽

Phanithi Prakash Babu

Keyword(s):

Cerebral Ischemia ◽

Caspase 3 ◽

Mapk Pathway ◽

Protective Role ◽

Akt Signaling ◽

Sirtuin 1 ◽

Neurological Dysfunction ◽

Dependent Manner ◽

Erk Mapk

AbstractCerebral ischemia (CI) is a severe cause of neurological dysfunction and mortality. Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders. The present study aims to investigate the protective role of SIRT1 after CI in experimental young and aged rats and humans. Also, the study examines the possible regulatory mechanisms of neuronal death in CI settings. Immunoblotting and immunohistochemistry were used to evaluate changes in the expression of SIRT1, JNK/ERK/MAPK/AKT signaling, and pro-apoptotic caspase-3 in experimental rats and CI patients. The study findings demonstrated that, in aged experimental rats, SIRT1 activation positively influenced JNK and ERK phosphorylation and modulated neuronal survival in AKT-dependent manner. Further, the protection conferred by SIRT1 was effectively reversed by JNK inhibition and increased pro-apoptotic caspase-3 expression. In young experimental rats, SIRT1 activation decreased the phosphorylation of stress-induced JNK, ERK, caspase-3, and increased the phosphorylation of AKT after CI. Inhibition of SIRT1 reversed the protective effect of resveratrol. More importantly, in human patients, SIRT1 expression, phosphorylation of JNK/ERK/MAPK/AKT signaling and caspase-3 were up-regulated. In conclusion, SIRT1 could possibly be involved in the modulation of JNK/ERK/MAPK/AKT signaling pathway in experimental rats and humans after CI.

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A follow-up study of child psychiatric clinic attenders with minor neurological dysfunction

European Child & Adolescent Psychiatry ◽

10.1007/bf02125568 ◽

1993 ◽

Vol 2 (3) ◽

pp. 136-145 ◽

Cited By ~ 2

Author(s):

Margot Völger ◽

Hans-Christoph Steinhausen ◽

Matthias Reitzle

Keyword(s):

Neurological Dysfunction ◽

Psychiatric Clinic ◽

Follow Up Study ◽

Child Psychiatric ◽

Minor Neurological Dysfunction

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Acute subdural hematoma

Journal of Neurosurgery ◽

10.3171/jns.1982.57.2.0254 ◽

1982 ◽

Vol 57 (2) ◽

pp. 254-257 ◽

Cited By ~ 46

Author(s):

Henry A. Shenkin

Keyword(s):

Computerized Tomography ◽

Subdural Hematoma ◽

Neurological Status ◽

Neurological Dysfunction ◽

Acute Subdural Hematoma ◽

Consecutive Series ◽

Content Type ◽

Subdural Hematomas ◽

Fine Print

✓ In a consecutive series of 39 cases of acute subdural hematoma (SDH), encountered since computerized tomography diagnosis became available, 61.5% were found to be the result of bleeding from a small cortical artery, 25.6% were of venous origin, 7.7% resulted from cerebral contusions, and 5% were acute bleeds into chronic subdural hematomas. Craniotomy was performed promptly on admission, but there was no difference in survival (overall 51.3%) between patients with arterial and venous bleeds. The only apparent factor affecting survival in this series was the preoperative neurological status: 67% of patients who were decerebrate and had fixed pupils prior to operation died. Of patients with less severe neurological dysfunction, only 20% failed to survive.

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