Cytotoxic Lesions of the Corpus Callosum (CLOCCs) Associated with SARS-CoV-2 Infection in West Africa (Côte d’Ivoire)

Background: Cytotoxic lesions of the corpus callosum (CLOCCs) represent a collection of disparate conditions that can cause a signal change in the corpus callosum, usually involving the splenium. CLOCCs is present in a variety of disorders, such as cerebral infarction, bleeding, multiple sclerosis, acute disseminated encephalomyelitis, glioblastoma, lymphoma, metabolic diseases, and infections. Since 2020, World Health Organization (W.H.O) defined Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, as a pandemic. Numerous CLOCCs cases have been reported in adults in particular in Japan, in China, and recently in children in Turkey associated with SARS-CoV-2. We report the first case of CLOCCs diagnosed in West Africa (Côte d’Ivoire) in an adult associated with SARS-CoV-2. Case Report: A 60 year-old-woman with a medical history of high blood pressure and diabetes, presented to the emergency department with confusion without fever. Neurological examination was normal apart from temporospatial disorientation. Brain magnetic resonance imaging (MRI) showed abnormal signals in the splenium of the corpus callosum (SCC). Forty-eight hours (48 h) after admission, the patient experienced a fever (temperature: 385˚C), several episodes of hypoglycemia (capillary blood glycemia levels below 0.5 g/l) and a dry cough. Lung CT imaging showed typical features with ground-glass opacities. Oropharyngeal swab was positive for SARS-CoV-2 on reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay. The clinical course was favorable. One month after disease onset, a follow-up Brain MRI showed considerable regression of SCC abnormal signal. The multiple episodes of hypoglycemia and SARS-COV 2 infection were incriminated as the causal factors. Conclusion: The improvement of the technical platform in our context of work gives us the possibility to identify the etiological factors of this rare clinico-radiological entity.

Ultrasound measurement of the corpus callosum and neural development of premature infants

Length and thickness of 152 corpus callosa Using ultrasonic diagnostic equipment with a were measured in neonates within 24 hours ot b^rtn. neonatal brain-specific probe, corpus callosum length and thickness of the genu, body, and splenium were measured on the standard mid-sagittal plane, and the anteroposterior diameter of the genu was measured in the coronal plane. Results showed that corpus callosum length as well as thickness of the genu and splenium increased with gesta- tional age and birth weight, while other measures did not. These three factors on the standard mid-sagittal plane are therefore likely to be suitable for real-time evaluation of corpus callosum de- velopment in premature infants using cranial ultrasound. Further analysis revealed that thickness of the body and splenium and the anteroposterior diameter of the genu were greater in male infants than in female infants, suggesting that there are sex differences in corpus callosum size during the neonatal period. A second set of measurements were taken from 40 premature infants whose ges- tational age was 34 weeks or less. Corpus callosum measurements were corrected to a gestational age of 40 weeks, and infants were grouped for analysis depending on the outcome of a neonatal behavioral neurological assessment. Compared with infants with a normal neurological assessment, corpus callosum length and genu and splenium thicknesses were less in those with abnormalities, indicating that corpus callosum growth in premature infants is associated with neurobehavioral development during the early extrauterine stage.

Polyethylene glycol restores axonal conduction after corpus callosum transection

Polyethylene glycol（PEG） has been shown to restore axonal continuity after peripheral nerve transection in animal models. We hypothesized that PEG can also restore axonal continuity in the central nervous system. In this current experiment, coronal sectioning of the brains of Sprague-Dawley rats was performed after animal sacrifice. 3Brain high-resolution microelectrode arrays（MEA） were used to measure mean firing rate（MFR） and peak amplitude across the corpus callosum of the ex-vivo brain slices. The corpus callosum was subsequently transected and repeated measurements were performed. The cut ends of the corpus callosum were still apposite at this time. A PEG solution was applied to the injury site and repeated measurements were performed. MEA measurements showed that PEG was capable of restoring electrophysiology signaling after transection of central nerves. Before injury, the average MFRs at the ipsilateral, midline, and contralateral corpus callosum were 0.76, 0.66, and 0.65 spikes/second, respectively, and the average peak amplitudes were 69.79, 58.68, and 49.60 μV, respectively. After injury, the average MFRs were 0.71, 0.14, and 0.25 spikes/second, respectively and peak amplitudes were 52.11, 8.98, and 16.09 μV, respectively. After application of PEG, there were spikes in MFR and peak amplitude at the injury site and contralaterally. The average MFRs were 0.75, 0.55, and 0.47 spikes/second at the ipsilateral, midline, and contralateral corpus callosum, respectively and peak amplitudes were 59.44, 45.33, 40.02 μV, respectively. There were statistically differences in the average MFRs and peak amplitudes between the midline and non-midline corpus callosum groups（P 〈 0.01, P 〈 0.05）. These findings suggest that PEG restores axonal conduction between severed central nerves, potentially representing axonal fusion.

Spinal Manipulation and Dynamic Neuromuscular Stabilization Care for a 4-Year-Old Patient with Agenesis of the Corpus Callosum

The purpose of this case study is to describe the chiropractic care of a 4-year-old male patient with agenesis of the corpus callosum. Methods: Chiropractic care plan consisted of weekly appointments with the inclusion of at-home exercises coupled with academic intervention of physical and occupational therapies and assistive gait devices. Functional changes were monitored via objective clinic findings, independent clinical examination, and parental observation. Results: Agitated flexion contracted non-weight bearing child with gastrointestinal dysfunction and developmentally shunted growth responds to co-managed chiropractic care. Focus on aiding structural balance helped improve the weight bearing movement and mobility, physical calmness and contentment, emotional and verbal communication, as well as gastointestinal function. Discussion: This therapeutic approach decreased aberrant posture and enhanced quality of life. Conclusion: Chiropractic care in combination with academic intervention improved this child’s postural abnormalities, attitude, and cognitive development warranting consideration in subsequent care investigation.

Clinical features of hereditary spastic paraplegia with thin corpus callosum: report of 5 Chinese cases

Background Hereditary spastic paraplegia is a clinically and genetically heterogeneous group of neurodegenerative disorders of the motor system, characterized by slowly progressive spasticity and weakness of the lower extremities. This study was conducted to investigate the clinical features of hereditary spastic paraplegia with thin corpus callosum (HSP-TCC). Methods Clinical data from five patients and thirty-five previously published case reports of HSP-TCC were analyzed retrospectively. Results Most patients were adolescents at the onset of the disease, presenting with spastic paraparesis of the lower limbs and mental impairment. Some patients also had other clinical features, including spasticity of the upper limbs, cerebellar ataxia, and sensory disturbances. Cranial MRIs of the five patients revealed an extremely thin corpus callosum, sometimes with widened cerebral sulci and ventricles, as well as with cerebellar and cerebral atrophy. Conclusion The main clinical features of HSP-TCC include slowly progressive spastic paraplegia, mental impairment during the second decade of life, and an extremely thin corpus callosum as shown on cranial MRIs.

Clinical Analysis of Children with Corpus Callosum Pressure Lesion Syndrome

Objective The aim of the study was to investigate the clinical features,imaging features,and prognosis of splenium of the corpus callosum in children in order to improve the clinical understanding.Methods The clinical data and imaging data of 30 children with splenium of the corpus callosum treated in Xiamen Children’s Hospital from June 2017 to October 2019 were retrospectively analyzed.Results Thirty children aged from 19 months to 12 years,with an average age of 5.4 years were included in the study;all had fever and other prodromal infections at acute onset,including 15 cases of respiratory tract infection,9 cases of digestive tract infection,and 6 cases of central nervous system infection.According to cranial magnetic resonance imaging(MRI)findings,23 cases had type I syndrome and 7 cases had type II syndrome;23 children had clinical symptoms disappeared after 1 week,7 children had clinical symptoms disappeared after 1 month,and 23 children had the abnormal signal disappeared after 2 weeks of reexamination,and the abnormal signal disappeared completely after 1 month of reexamination in 7 children.Conclusion Central nervous system infection is also a predisposing factor for the pressor syndrome of the corpus callosum in children in addition to upper respiratory tract infection and gastrointestinal tract infection,and all children have good prognosis.

Protective effects of carnosine on white matter damage induced by chronic cerebral hypoperfusion

Carnosine is a dipeptide that scavenges free radicals, inhibits infammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. Therefore, we hypothesized that carnosine would also protect against white matter damage caused by subcortical ischemic injury. White matter damage was induced by right unilateral common carotid artery occlusion in mice. The animals were treated with 200, 500 or 750 mg/kg carnosine by intraperitoneal injection 30 minutes before injury and every other day after injury. Then, 37 days later, Klfiver-Barrera staining, toluidine blue staining and immunofluorescence stain- ing were performed. Carnosine （200, 500 mg/kg） substantially reduced damage to the white matter in the corpus callosum, internal capsule and optic tract, and it rescued expression of myelin basic protein, and alleviated the loss of oligodendrocytes. However, carnosine at the higher dose of 750 mg/kg did not have the same effects as the 200 and 500 mg/kg doses. These findings show that carnosine, at a particular dose range, protects against white matter damage caused by chronic cerebral ischemia in mice, likely by reducing oligodendroglial cell loss.

Association between Alzheimer's disease pathogenesis and early demyelination and oligodendrocyte dysfunction

The APPSwe/PSEN1 dE9（APP/PS1） transgenic mouse model is an Alzheimer＇s disease mouse model exhibiting symptoms of dementia, and is commonly used to explore pathological changes in the development of Alzheimer＇s disease. Previous clinical autopsy and imaging studies suggest that Alzheimer＇s disease patients have white matter and oligodendrocyte damage, but the underlying mechanisms of these have not been revealed. Therefore, the present study used APP/PS1 mice to assess cognitive change, myelin loss, and corresponding changes in oligodendrocytes, and to explore the underlying mechanisms. Morris water maze tests were performed to evaluate cognitive change in APP/PS1 mice and normal C57 BL/6 mice aged 3 and 6 months. Luxol fast blue staining of the corpus callosum and quantitative reverse transcription-polymerase chain reaction（q RT-PCR） for myelin basic protein（MBP） mRNA were carried out to quantify myelin damage. Immunohistochemistry staining for NG2 and qRT-PCR for monocarboxylic acid transporter 1（MCT1） mRNA were conducted to assess corresponding changes in oligodendrocytes. Our results demonstrate that compared with C57 BL/6 mice, there was a downregulation of MBP mRNA in APP/PS1 mice aged 3 months. This became more obvious in APP/PS1 mice aged 6 months accompanied by other abnormalities such as prolonged escape latency in the Morris water maze test, shrinkage of the corpus callosum, upregulation of NG2-immunoreactive cells, and downregulation of MCT1 mRNA. These findings indicate that the involvement of early demyelination at 3 months and the oligodendrocyte dysfunction at 6 months in APP/PS1 mice are in association with Alzheimer＇s disease pathogenesis.

Clinical Characteristics of H1N1 Influenza A-Associated Mild Encephalopathy with Reversible Splenial Lesion: 4 Pediatric Cases

Objective Mild encephalopathy with reversible splenial lesion(MERS)is associated with a variety of infections and anti-epileptic drug withdrawal.Here we report the clinical characteristics of H1N1 influenza A-associated MERS based on our experience of four pediatric cases.Methods A detailed retrospective analysis of four patients with H1N1 influenza A-associated MERS was performed at Guangzhou Women and Children’s Medical Center.Results All patients exhibited mild influenza-like illness and seizures.Three patients presented with a new-onset seizure with fever after 5 years of age.75%patients had altered mental status.For all four patients,influenza A(H1N1)viral RNA was detected in throat swab specimens at least twice.Brain magnetic resonance images revealed similar ovoid lesions in the corpus callosum,mainly in the splenium and for one patient in the splenium and genu of the corpus callosum.Only one patient had an abnormal electroencephalogram tracing.Cells and protein in the cerebrospinal fluid were normal in all patients.All patients received oseltamivir and one patient received intravenous immunoglobulin.As a result,all patients fully recovered after 2 months and showed no neurologic sequelae at discharge.Conclusion This case series provides insight towards clinical features of H1N1 influenza A-associated MERS.

Hypothermia selectively protects the anterior forebrain mesocircuit during global cerebral ischemia

Hypothermia is an important protective strategy against global cerebral ischemia following cardiac arrest.However,the mechanisms of hypothermia underlying the changes in different regions and connections of the brain have not been fully elucidated.This study aims to identify the metabolic nodes and connection integrity of specific brain regions in rats with global cerebral ischemia that are most affected by hypothermia treatment.18F-fluorodeoxyglucose positron emission tomography was used to quantitatively determine glucose metabolism in different brain regions in a rat model of global cerebral ischemia established at 31–33℃.Diffusion tensor imaging was also used to reconstruct and explore the brain connections involved.The results showed that,compared with the model rats established at 37–37.5℃,the rat models of global cerebral ischemia established at 31–33℃had smaller hypometabolic regions in the thalamus and primary sensory areas and sustained no obvious thalamic injury.Hypothermia selectively preserved the integrity of the anterior forebrain mesocircuit,exhibiting protective effects on the brain during the global cerebral ischemia.The study was approved by the Institutional Animal Care and Use Committee at Capital Medical University(approval No.XW-AD318-97-019)on December 15,2019.

Expression of NG2 and platelet-derived growth facto receptor alpha in the developing neonatal rat brain

Platelet-derived growth factor receptor alpha （PDGFRct） is a marker of oligodendrocyte precursor cells in the central nervous system. NG2 is also considered a marker of oligodendrocyte precursor cells. However, whether there are differences in the distribution and morphol- ogy of oligodendrocyte precursor cells labeled by NG2 or PDGFRa in the developing neonatal rat brain remains unclear. In this study, by immunohistochemical staining, NG2 positive （NG2＋） cells were ubiquitous in the molecular layer, external pyramidal layer, internal pyramidal layer, and polymorphic layer of the cerebral cortex, and corpus callosum, external capsule, piriform cortex, and medial septal nucleus. NG2~ cells were stellate or fusiform in shape with long processes that were progressively decreased and shortened over the course of brain development. The distribution and morphology of PDGFRct positive （PDGFRa＋） cells were coincident with NG2＋ cells. The co- localization of NG2 and PDGFRu in the cell bodies and processes of some cells was confirmed by double immunofluorescence labeling. Moreover, cells double-labeled for NG2 and PDGFRa were predominantly in the early postnatal stage of development. The numbers of NG2＋/PDGFRa＋ cells and PDGFRa＋ cells decreased, but the number of NG2＋ cells increased from postnatal days 3 to 14 in the developing brain. In addition, amoeboid microglial cells of the corpus callosum, newborn brain macrophages in the normal developing brain, did not express NG2 or PDGFRu, but NG2 expression was detected in amoeboid microglia after hypoxia. The present results suggest that NG2 and PDGFRct are specific markers of oligodendrocyte precursor cells at different stages during early development. Additionally, the NG2 protein is involved in inflammatory and pathological processes of amoeboid microglial cells.

Lagged Coherence of Photon Emissions and Spectral Power Densities between the Cerebral Hemispheres of Human Subjects during Rest Conditions: Phase Shift and Quantum Possibilities

Photon counts about 15 cm from the left and right sides of the head while subjects sat quietly during baseline conditions within a hyper-dark chamber were measured by photomultiplier units. Lag/lead analyses for photon emissions between the two hemispheres indicated a weak but statistically significant correlation between the amplitude fluctuations that were separated by about 800 to 900 ms. Analyses of the spectral power densities of photon amplitude variations from the left and right hemispheres revealed peak values between 2 and 3 Hz which were equivalent to a difference of about 900 ms. The radiant flux densities were estimated to be in the order of 10?12 W?m?2 and to include the equivalence of about 107 neurons. Our calculations, which accounted for the small magnitude of the strength of the interhemispheric coefficients, suggest that the coherence could be strongly correlated with processes associated with the unmyelinated axons with diameters between 400 to 800 nm, the visible wavelengths, within the corpus callosum. When the ratio of the phase shift was applied to the Aharanov-Bohm equation, the time required for a photon-related electron to be within a cerebral magnetic field was the same duration as a single orbit of an electron and a photon’s traversal latency across a neuronal plasma membrane. We suggest that the peak photon decoherence between the two cerebral hemispheres may reveal a neuronal-quanta substrate to the conditions associated with consciousness.

Aicardi syndrome:Neonatal diagnosis by means of transfontanellar ultrasound

Aicardi syndrome is a rare genetic disease characterized by a characteristic classical trio of neurological clinical abnormalities(spasms),agenesis of the corpus callosum and ophthalmological abnormalities(chorioretinal lacunae).The diagnosis can be suspected by prenatal ultrasound with color Doppler identifying the agenesis of the corpus callosum.Usually,the diagnosis is confirmed in the neonate period by transfontanellar ultrasound and ophthalmological examination.We present a case of newborn with Aicardi syndrome,being the transfontanellar identified partial dysgenesis of the corpus callosum and a cyst in the inter-hemispheric fissure.Ophthalmological examination showed bilateral chorioretinal lacunae.