Suspected myelinolysis following rapid correction of hyponatremia in a dog

1999 ◽  
Vol 35 (6) ◽  
pp. 493-497 ◽  
Author(s):  
RK Churcher ◽  
AD Watson ◽  
A Eaton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Dysfunction ◽  
Laboratory Findings ◽  
Neurological Signs ◽  
Therapeutic Guidelines ◽  
Chronic Hyponatremia ◽  
Iatrogenic Damage ◽  
Gastrointestinal Parasitism ◽  
Rapid Correction

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.

scholarly journals Comparison of clinical features of pulmonary cryptococcosis with and without central nervous system involvement in China

2021 ◽  
Vol 49 (2) ◽  
pp. ???
Author(s):  
Xinying Xue ◽  
Xuelei Zang ◽  
Lifeng Wang ◽  
Dongliang Lin ◽  
Tianjiao Jiang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Central Nervous System ◽  
Nervous System ◽  
Clinical Features ◽  
Central Nervous System Involvement ◽  
Pulmonary Cryptococcosis ◽  
Cns Involvement ◽  
Laboratory Findings ◽  
Logistic Regression Models ◽  
Presenting Symptoms

Objective This study aimed to compare the clinical features of pulmonary cryptococcosis (PC) in patients with and without central nervous system (CNS) involvement. Methods We retrospectively reviewed demographics, presenting symptoms, radiographic features, and laboratory findings of patients diagnosed with PC in 28 hospitals from 2010 to 2019. Risk factors for CNS involvement were analyzed using logistic regression models. Result A total of 440 patients were included, and 36 (8.2%) had CNS involvement. Significant differences in fever, headache, and chills occurred between the two groups (overall and with/without CNS involvement) for fever (17.8% [78/440]; 52.8% vs. 14.6% of patients, respectively), headache (4.5% [20/440]; 55.6% vs. 0% of patients, respectively), and chills (4.3% [19/440]; 13.9% vs. 3.5% of patients, respectively). The common imaging manifestation was nodules (66.4%). Multivariate analysis showed that cavitation (adjusted odds ratio [AOR] = 3.552), fever (AOR = 4.182), and headache were risk factors for CNS involvement. Routine blood tests showed no differences between the groups, whereas in cerebrospinal fluid the white blood cell count increased significantly and glucose decreased significantly. Conclusion In patients with PC, the risk of CNS involvement increases in patients with headache, fever, and cavitation; these unique clinical features may be helpful in the diagnosis.

scholarly journals Superficial siderosis of the central nervous system is a rare and possibly underdiagnosed disorder

2017 ◽  
Vol 75 (2) ◽  
pp. 92-95 ◽  
Author(s):  
Yara Dadalti Fragoso ◽  
Tarso Adoni ◽  
Joseph Bruno Bidin Brooks ◽  
Sidney Gomes ◽  
Marcus Vinicius Magno Goncalves ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Disease Onset ◽  
Clinical Findings ◽  
Neurological Dysfunction ◽  
Superficial Siderosis ◽  
Blood Products ◽  
The Central Nervous System ◽  
Magnetic Resonance Imaging Mri ◽  
Intermittent Bleeding

ABSTRACT Superficial siderosis (SS) of the central nervous system (CNS) is a rare and possibly underdiagnosed disorder resulting from chronic or intermittent bleeding into the subarachnoid space, leading to deposition of blood products in the subpial layers of the meninges. Magnetic resonance imaging (MRI) shows a characteristic curvilinear pattern of hypointensity on its blood-sensitive sequences. Methods Series of cases collected from Brazilian centers. Results We studied 13 cases of patients presenting with progressive histories of neurological dysfunction caused by SS-CNS. The most frequent clinical findings in these patients were progressive gait ataxia, hearing loss, hyperreflexia and cognitive dysfunction. The diagnoses of SS-CNS were made seven months to 30 years after the disease onset. Conclusion SS-CNS is a rare disease that may remain undiagnosed for long periods. Awareness of this condition is essential for the clinician.

Acute reversible toxic encephalopathy during capecitabine and oxaliplatin treatment

2017 ◽  
Vol 25 (2) ◽  
pp. 497-501 ◽  
Author(s):  
João Godinho ◽  
Mafalda Casa-Nova ◽  
Teresa Mesquita ◽  
Maria João Baptista ◽  
Francisco Araújo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Findings ◽  
Neurological Dysfunction ◽  
Toxic Encephalopathy ◽  
Central Nervous System Toxicity ◽  
Cerebellar Dysfunction ◽  
Oxaliplatin Treatment ◽  
Tumor Involvement ◽  
The Central Nervous System

Introduction Capecitabine is a fluoropyrimidine commonly used in the treatment of colorectal cancer which may cause central nervous system toxicity, namely cerebellar dysfunction. Case report We describe a 77-year-old man undergoing adjuvant treatment of colon cancer with capecitabine and oxaliplatin who presented with acute cerebellar ataxia and encephalopathy that progressed to coma. Diagnosis of toxic encephalopathy was made after the exclusion of alternative causes of neurological dysfunction and complete resolution of clinical findings with permanent discontinuation of chemotherapy. Discussion When patients with cancer develop symptoms and signs of central nervous dysfunction, metabolic and infectious causes plus tumor involvement of central nervous system must be sought. However, chemotherapy may also cause toxicity to the central nervous system. Capecitabine is no exception, although cerebellar dysfunction is rarely reported. Conclusion Although rare, capecitabine-induced encephalopathy may be severe and physicians should be aware of this possible side effect.

MENINGOENCEPHALITIS AND LABORATORY EVIDENCE OF TRIPLE INFECTION WITH CALIFORNIA ENCEPHALITIS VIRUS, ECHOVIRUS II, AND MUMPS

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 680-684 ◽  
Author(s):  
Henry H. Balfour ◽  
Gregory L. Seifert ◽  
Milton H. Seifert ◽  
Paul G. Quie ◽  
Charlene K. Edelman ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
Central Nervous System Disease ◽  
Encephalitis Virus ◽  
Laboratory Findings ◽  
Laboratory Evidence ◽  
System Disease ◽  
Triple Infection ◽  
Echovirus Type

This report emphasizes that in acute central nervous system disease, multiple viral agents may be implicated in the same patient. A 6-year-old girl with meningoencephalitis had laboratory evidence for simultaneous or closely spaced infections with California encephalitis virus, echovirus type 11, and mumps. Documentation of the finding of triple viral infection was based on at least two laboratory findings for each agent. The patient lived in an area where California encephalitis was prevalent.

Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system

1978 ◽  
Vol 39 (3) ◽  
pp. 501-513 ◽  
Author(s):  
C. Fehling ◽  
Margaretha JÄgerstad ◽  
B. Åkesson ◽  
J. Axelsson ◽  
A. Brun
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid ◽  
Motor Nerve ◽  
Vitamin B12 Deficiency ◽  
Neurological Dysfunction ◽  
Vitamin B ◽  
Deficient Diet ◽  
Neurological Signs ◽  
The Central Nervous System

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12–15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water.2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system.3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency.4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats.5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.

Resection of a cystic brainstem hemangioblastoma via a retrosigmoid approach

2014 ◽  
Vol 36 (v1supplement) ◽  
pp. 1 ◽  
Author(s):  
Brian Lee ◽  
Yvette D. Marquez ◽  
Steven L. Giannotta
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Dysfunction ◽  
Neural Pathways ◽  
Technical Challenge ◽  
Cystic Component ◽  
Complete Surgical Resection ◽  
Close Proximity ◽  
The Central Nervous System ◽  
Vascular Structures

Lesions of the brainstem pose a technical challenge due to their close proximity to critical vascular structures, neural pathways, and nuclei. Hemangioblastomas are rare lesions of the central nervous system and can cause significant neurological dysfunction, primarily due to enlargement of the cystic component. This is especially relevant when hemangioblastomas occur in eloquent brainstem regions. However, the outcomes after hemangioblastoma resection are good if complete surgical resection of the tumor of the mural nodule, can be achieved. This video demonstrates the excision of a brainstem hemangioblastoma via a left retrosigmoid craniotomy under Stealth guidance.The video can be found here: http://youtu.be/bCkuaPwMV20.

scholarly journals MiR-124 and Small Molecules Synergistically Regulate the Direct Generation of Neuronal Cells from Rat Cortical Reactive Astrocytes

2020 ◽  
Author(s):  
Yangyang Zheng ◽  
Zhehao Huang ◽  
Jinying Xu ◽  
Kun Hou ◽  
Yifei Yu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Small Molecules ◽  
Expression Patterns ◽  
Cholinergic Neurons ◽  
Reactive Astrocytes ◽  
Neurological Dysfunction ◽  
Neuronal Regeneration ◽  
Neuronal Markers ◽  
Hes1 Expression

Abstract Background：Irreversible neuron loss caused by central nervous system injuries usually lead to persistent neurological dysfunction. Reactive astrocytes, because of their high proliferative capacity, proximity to neuronal lineage, and significant involvement in glial scarring, are ideal starting cells for neuronal regeneration. Having previously identified several small molecules as important regulators of astrocyte-to-neuron reprogramming, our aim in this study was to explore whether other small molecules and miR-124, a key neural differentiation mediator, could co-regulate reactive astrocyte-to-neuron conversion.Methods: MiR-124, ruxolitinib, SB203580, and forskolin were used to induce postnatal rat cortex reactive astrocytes, and the neuronal phenotype of the induced cells was characterised. To understand the genetic changes, RNA-sequencing analyses were performed on reactive astrocytes, induced neurons, and rat neurons, and the mechanisms underlying the regulatory role of miR-124 during the neuronal conversion was explored.Results：MiR-124, ruxolitinib, SB203580, and forskolin could co-convert rat cortical reactive astrocytes into neurons. The induced cells had reduced astroglial properties, displayed typical neuronal morphologies, and expressed neuronal markers, reflecting 25.9% of cholinergic neurons and 22.3% of glutamatergic neurons. Gene analysis revealed that induced neuron gene expression patterns were more similar to that of primary neurons than of initial reactive astrocytes. On the molecular level, miR-124-driven neuronal differentiation of reactive astrocytes was via targeting of the SOX9-NFIA-HES1 axis to inhibit HES1 expression.Conclusions：Providing a novel approach for inducing endogenous rat cortical reactive astrocytes into neurons by co-regulation involving miR-124 and three small molecules, our research has potential implications for inhibiting glial scar formation and promoting neuronal regeneration after central nervous system injury or disease.

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