Brainstem Lesions Research Articles

2-Hydroxyglutarate magnetic resonance spectroscopy in adult brainstem glioma.

Adult brainstem gliomas (BSGs) are rare tumors of the CNS that are poorly understood. Upregulation of the oncometabolite 2-hydroxyglutarate (2HG) in the tumor indicates the mutation of isocitrate dehydrogenase (IDH), which can be detected by magnetic resonance spectroscopy (MRS). Although histological examination is required for the definitive diagnosis of BSG, 2HG-optimized MRS (2HG-MRS) may be useful, considering the difficult nature of brainstem lesion biopsy. The aim of this study was to evaluate the utility of 2HG-MRS for diagnosing IDH-mutant adult BSG. Patients with a radiographically confirmed brainstem tumor underwent 3T MRS. A single voxel was set in the lesion with reference to the T2 or fluid-attenuated inversion recovery image and analyzed according to the 2HG-tailored MRS protocol (point-resolved spectroscopic sequence; echo time 35 msec). All patients underwent intraoperative navigation-guided or CT-guided stereotactic biopsy for histopathological diagnosis. The status of IDH and H3K27M mutations was confirmed by immunohistochemistry and direct DNA sequencing. In addition, the authors examined the relationship between patients' 2HG concentrations and survival time. Ten patients (7 men, 3 women; median age 33.5 years) underwent 2HG-MRS and biopsy. Four patients had an H3K27M mutation and 4 had an IDH1 mutation (1 R132H canonical IDH mutation, 2 R132S and 1 R132G noncanonical IDH mutations). Two had neither H3K27M nor IDH mutations. The H3K27M and IDH mutations were mutually exclusive. Most tumors were located in the pons. There was no significant radiological difference between mutant H3K27M and IDH on a conventional MRI sequence. A 2HG concentration ≥ 1.8 mM on MRS demonstrated 100% (95% CI 28%-100%) sensitivity and 100% (95% CI 42%-100%) specificity for IDH-mutant BSG (p = 0.0048). The median overall survival was 10 months in IDH-wild-type BSG patients (n = 6) and could not be estimated in IDH-mutant BSG patients (n = 4) due to the small number of deaths (p = 0.008). 2HG-MRS demonstrated high sensitivity and specificity for the prediction of IDH-mutant BSG. In addition, 2HG-MRS may be useful for predicting the prognosis of adult BSG patients.

Caffeine alleviates anxiety-like behavior and brainstem lesions in a rotenone-induced rat model of Parkinson's disease

BackgroundParkinson's disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms. In 2016, approximately 6.1 million individuals were affected by PD, with 211,296 deaths attributed to the disease. The understanding of PD initially came from the observation of dopaminergic system alterations in a specific region of the brainstem, indicating that the core motor and non-motor features of PD are closely associated with brainstem dysfunction. The primary treatment approach for PD revolves around dopamine replacement, as many of the symptoms are responsive to this therapeutic intervention. However, long-term administration of this approach is linked to several complications, and a definitive gold-standard therapy for PD is yet to be identified. The pharmacological management of PD has been challenging and inconsistent, mainly due to the unclear underlying cause of the disease. This study aims to evaluate the effects of caffeine on the brainstem of rats with PD induced by rotenone. MethodologyFifty adult male Wistar rats weighing between 150 and 200 g were used in this study. The rats were randomly divided into five groups of ten rats each: Vehicle Group, Rotenone-only treated Group (rotenone only treated with 3 mg/kg, intraperitoneal administration [IP]), Preventive Group (caffeine 30 mg/kg + rotenone 3 mg/kg, IP), Curative Group (rotenone 3 mg/kg + caffeine 30 mg/kg, IP), and Caffeine only treated Group (caffeine only treated with 30 mg/kg, IP). The animals underwent neurobehavioral assessments, followed by sacrifice. The brains were then excised, weighed, and processed histologically. Appropriate brain sections were taken and processed. Photomicrographs were obtained, morphometric and statistical analysis was performed using an Omax LED digital ResultsThe results demonstrated a significant (p < 0.05) reduction in body weight and relative brain weight, which were increased by caffeine treatments. Rotenone administration led to histological changes similar to those observed in PD, including neuronal structural derangement, degenerated nerve fibers, loss of myelinated neurons, and Nissl substance, as well as downregulation in the expressions of NRF2 and TH in the midbrain. However, these pathological features were counteracted or ameliorated by caffeine treatment. ConclusionOur study contributes additional evidence to the growing body of research supporting the therapeutic potential of caffeine in Parkinson's disease (PD). The results underscore the neuroprotective properties of caffeine and its capacity to mitigate oxidative stress by modulating TH (tyrosine hydroxylase) and cytoplasmic NRF2 (nuclear factor erythroid 2-related factor 2) in the mesencephalon. These findings suggest that caffeine holds promise as a viable treatment option for PD.

Memories without Survival: Personal Identity and the Ascending Reticular Activating System.

Lockean views of personal identity maintain that we are essentially persons who persist diachronically by virtue of being psychologically continuous with our former selves. In this article, I present a novel objection to this variant of psychological accounts, which is based on neurophysiological characteristics of the brain. While the mental states that constitute said psychological continuity reside in the cerebral hemispheres, so that for the former to persist only the upper brain must remain intact, being conscious additionally requires that a structure originating in the brainstem-the ascending reticular activating system-be functional. Hence, there can be situations in which even small brainstem lesions render individuals irreversibly comatose and thus forever preclude access to their mental states, while the neural correlates of the states themselves are retained. In these situations, Lockeans are forced to regard as fulfilled their criterion of diachronic persistence since psychological continuity, as they construe it, is not disrupted. Deeming an entity that is never again going to have any mental experiences to be a person, however, is an untenable position for a psychological account to adopt. In their current form, Lockean views of personal identity are therefore incompatible with human neurophysiology.

Primary CNS T-Cell Lymphoma Presenting as a Brainstem Lesion in a Young Female

Primary CNS T-Cell Lymphoma Presenting as a Brainstem Lesion in a Young Female

Oligoclonal Band Status and Features of Radiological and Clinical Findings in Patients with Multiple Sclerosis in Lithuania.

Background and Objectives: Multiple sclerosis (MS) is a widely spread and debilitating disease with 2.8 million people worldwide currently affected. However, the exact pathogenesis of the disease and its progression remains incompletely understood. According to the revised McDonald criteria, cerebrospinal fluid oligoclonal bands (CSF OCBs) magnetic resonance imaging (MRI) results, in conjunction with clinical presentation, remain the gold standard of MS diagnostics. Therefore, this study aims to evaluate the association between CSF OCB status and features of radiological and clinical findings in patients with multiple sclerosis in Lithuania. Materials and Methods: The selection of 200 MS patients was performed in order to find associations between CSF OCB status, MRI data and various disease features. The data were acquired from outpatient records and a retrospective analysis was performed. Results: OCB positive patients were diagnosed with MS earlier and had spinal cord lesions more frequently than OCB negative patients. Patients with lesions in the corpus callosum had a greater increase in the Expanded Disability Status Scale (EDSS) score between their first and last visit. Patients with brainstem lesions had higher EDSS scores during their first and last visit. Even so, the progression of the EDSS score was not greater. The time between the first symptoms and diagnosis was shorter for patients who had juxtacortical lesions than patients who did not. Conclusions: CSF OCBs and MRI data remain irreplaceable tools when diagnosing multiple sclerosis as well as prognosing the development of the disease and disability.

A case study of left visual neglect after right pontine lesion: pathophysiological evidence for the infratentorial involvement in human visual attention.

Hemispatial neglect, the inability to attend to the contralesional side of space, is the most common disturbance of visuospatial attention. Both hemispatial neglect and visuospatial attention are typically associated with extended cortical networks. Nevertheless, recent accounts challenge this so-called corticocentric view and postulate the participation of structures well beyond the telencephalic cortex, in particular advocating the role of the brainstem. However, to the best of our knowledge, hemispatial neglect after a brainstem lesion has not yet been described. We describe, for the first time in a human, the occurrence and remission of contralesional visual hemispatial neglect after a focal lesion in the right pons. Hemispatial neglect was assessed by means of video-oculography during free visual exploration, a very sensitive and established method, and its remission was followed up until 3 wk after stroke. Moreover, by means of a lesion-deficit approach complemented by imaging, we identify a pathophysiological mechanism involving the disconnection of cortico-ponto-cerebellar and/or tecto-cerebellar-tectal pathways passing through the pons. Our findings offer, for the first time in a human, causal, lesion-based support for recent seminal accounts postulating the role of infratentorial structures participating in the activity of cerebral cortical attentional networks mediating attentional processes.NEW & NOTEWORTHY Visuospatial attention and its most common disturbance, hemispatial neglect, are typically associated with extended cortical networks. However, recent accounts challenge this corticocentric view and advocate the role of infratentorial structures. We describe, for the first time in a human, the occurrence of contralesional visual hemispatial neglect after a focal lesion in the right pons. We provide causal, lesion-based evidence for a pathophysiological mechanism involving the disconnection of cortico-ponto-cerebellar and/or tecto-cerebellar-tectal pathways passing through the pons.

Metabolic inflexibility and unusual catabolism in Leigh-like syndrome due to m.10191T>C

Hypercatabolism is a well-known feature of mitochondrial diseases but some patients may present with hypometabolism, as the following case. Case report using standard investigation methods. The patient is a 32 years-old female with a Leigh-like syndrome due to the mtDNA variant m.10191T>C in MT-ND3. Leigh-like syndrome is characterized by symmetric basal ganglia or brainstem lesions plus involvement of organs other than the brain. The patient presented with hypometabolism, which did not respond to ketogenic diet but responded to fasting. The patient showed a Warburg-like effect, which resulted in reliance on glucose due to the exclusion of oxidative phosphorylation with an extremely low VO2max. The patient only entered substantial ketosis when all gluconeogenic substrates were removed. Prolonged survival in the index patient may have possibly resulted from this previously unreported protective mechanism to reduce oxidative stress. The unusual Warburg-like phenomenon was interpreted as a possible mechanism of patients with a mitochondrial disease to survive into adulthood. This case shows that mitochondrial disease can manifest with hypometabolism and that an unusual Warburg-like effect may be responsible in some patients with mitochondrial disease to survive into adulthood.

Impact of socioeconomics and race on clinical follow-up and trial enrollment and adherence in cerebral cavernous malformation

ObjectivesCerebral cavernous malformation (CCM) affects more than a million Americans but advanced care for symptomatic lesions and access to research studies is largely limited to referral academic centers Materials and methodsA cohort of CCM patients screened for research studies at an accredited center of excellence for CCM was analyzed. Demographics, lesion location, history of hemorrhage, insurance type and area of deprivation index (ADI) were collected. Primary outcomes were clinical follow-up within a year from initial evaluation, and enrollment and adherence in clinical trials among eligible subjects ResultsA majority (52.8%) of CCM patients evaluated had a high socioeconomic status (SES) (ADI 1-3), and only 11.5% were African American. Patients who had a symptomatic bleed were more likely to follow-up (p=0.01), and those with brainstem lesion were more likely to enroll/adhere in a clinical trial (p=0.02). Rates of clinical follow-up were similar across different ADI groups, insurance coverage and race. Patients who were uninsured/self-paying, and African Americans were more likely to decline/drop from clinical trials (OR 2.4, 95% CI 0.46-10.20 and OR 2.2, 95% CI 0.33-10.75, respectively), but differences were not statistically significant ConclusionsAccess of disadvantaged patients to center of excellence care and research remains limited despite geographic proximity to their community. Patients with lower SES and African Americans are as likely to follow-up clinically, but there were trends of differences in enrollment/adherence in clinical trials. Mitigation efforts should target systemic causes of low access to specialized care among uninsured and African American patients.

Study on posterior circulatory stroke characteristics and clinico-radiological imaging

Background: Stroke research and clinical trials have focused mainly on anterior circulation stroke (ACS). Since clinical characteristics, mechanisms, and risk factors of posterior circulation stroke (PCS) have been reported different from ACS, more PCS studies are required. Methods: A Prospective, observational, Clinical study. All patients presenting to the department of general medicine and neurology of saveetha medical college from august 2021 to January 2023 with new onset neuro-deficit. Inclusion criteria is patients age 18 years or older and Clinical profile, radiological finding which is suggestive of acute PCS. Radiological imaging was done in detail to assess the artery involved and area affected. Results: Most common associated risk factors were hypertension (61%), alcoholism (33%) and smoking (32%). Most common presenting clinical symptoms of cases with PCS are giddiness (59%), left/ right sided weakness (48%). Posterior cerebral artery was involved in 45% of the patients. The next common involvement was that of the posterior inferior cerebellar artery (38%). Most common area involved was brainstem, cerebellum. Conclusions: This study describes the pattern of risk factors and clinical characteristics of PCS. Males were affected more than females. Age group commonly involved was above sixty years. Hypertension, alcoholism, diabetes and smoking contributed the major risk factors. Giddiness was commonest symptom at the onset. Most of the patients had clinical signs of cerebellum and brainstem lesions. The territory commonly involved was mid-brain, cerebellum, thalamus, occipital and temporal lobes.

A Case of Neural Integrator Failure in Vitamin B1 Deficiency. (P1-9.004)

<h3>Objective:</h3> Case Report <h3>Background:</h3> The nucleus prepositus hypoglossi (NPH) and medial vestibular nuclei (MVN) are two closely related neural integrators situated in the brainstem responsible for horizontal conjugate eye movement. Thiamine deficiency, a hallmark of Wernicke’s encephalopathy, affects the MVN to a greater extent. We report a case of impaired horizontal gaze holding post-sleeve gastrectomy secondary to Vitamin B1 deficiency. <h3>Design/Methods:</h3> A 24-year-old female presented with new onset diplopia on lateral gaze, dizziness, and lower limb distal paraesthesia eight weeks post-sleeve gastrectomy. Examination revealed conjugate eye movements and horizontal gaze-holding failure bilaterally, with intact convergence and vertical gaze. Normal discs were observed on fundoscopy with no retinal haemorrhages, and visual acuity preserved. She had a normal mental state with mild sensory ataxia. Reflexes were present and symmetrical. <h3>Results:</h3> Cerebrospinal fluid analysis was normal, and MRI Brain showed no acute infarction, haemorrhage, or brainstem lesions. Folate, Vitamin B6, B12, and HbA1c levels were within normal range, with a negative infective screen. Vitamin B1 level was found to be low at 44.3nmol/L (normal range: 66.5–200nmol/L). She was commenced on high-dose intravenous thiamine for one week with symptomatic improvement in diplopia and subsequently discharged on long-term thiamine supplementation. <h3>Conclusions:</h3> The high metabolic requirements of MVN neurons responsible for high acceleration horizontal vestibulo-ocular reflex (VOR) is postulated to account for the selective vulnerability to thiamine deprivation. This case highlights an unusual presentation of disruption in horizontal gaze-holding mechanisms through failure of neural integrators, particularly the MVN, in the setting of Vitamin B1 deficiency with preservation of vertical gaze. <b>Disclosure:</b> Dr. Chen has nothing to disclose. Dr. Warfield has nothing to disclose. Dr. Nannery has nothing to disclose. Dr. Togher has nothing to disclose. Dr. Yacoob has nothing to disclose.

Temporal Relationship of Breast Cancer and Paraneoplastic Neuromyelitis Optica Spectrum Disorder (NMOSD) (P13-5.001)

<h3>Objective:</h3> A systematic review and meta-analysis was conducted in order to characterize the temporal relationship between the diagnosis of neuromyelitis optica spectrum disorder (NMOSD) and breast cancer. <h3>Background:</h3> Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory and demyelinating disorder affecting the optic nerve and spinal cord more frequently than other parts of the central nervous system (CNS). NMOSD was recognized as a unique condition with a chronic, relapsing course after the identification of IgG-class antibodies that bind to the water channel aquaporin-4 (AQP4-IgG) in serum from individuals with NMO. Typically this is an idiopathic autoimmune disorder, although there is increasing evidence behind the expression of AQP4 antibodies in the setting of an underlying tumor with NMOSD manifesting as a paraneoplastic syndrome. <h3>Design/Methods:</h3> This systematic review and meta-analysis was completed in accordance PRISMA guidelines. A literature search was conducted on PubMed/PubMed Central/MEDLINE, Scopus, and ScienceDirect databases. The review was registered with PROSPERO (Registration ID: CRD42022352109). <h3>Results:</h3> The search strategy yielded a total of 10 records, from which 16 cases were identified. Triple-negative breast cancer was the most prevalent form of breast cancer. Seven cases recorded the presence of longitudinally extensive transverse myelitis (LETM) involving the cervical and thoracic cord. Five cases identified lesions on magnetic resonance imaging (MRI) within the brainstem. And four cases described lesions within the cerebrum and/or cerebellum. Intravenous methylprednisolone (IVMP) was the most common agent used in the acute management of NMOSD. On average the diagnosis of NMOSD occurred 1.4 months before that of breast cancer. <h3>Conclusions:</h3> NMOSD is a rare autoimmune condition that can occur in a paraneoplastic manner. The diagnosis of NMOSD precedes that of breast cancer with a mean time of 1.4 months. Triple-negative breast cancer is the most commonly identified subtype. Common MRI findings include LETM of the cervical and thoracic cord as well as brainstem lesions. <b>Disclosure:</b> Dr. Sivakumar has nothing to disclose. Dr. Srichawla has nothing to disclose. Dr. Cheraghi has nothing to disclose.

Ipsilateral weakness caused by ipsilateral stroke: A case series

IntroductionThere are few reported cases of ipsilateral weakness following ischemic or hemorrhagic stroke. In these rare cases, ipsilateral weakness is typically the result of damage to uncrossed components of the corticospinal tract (CST) which were recruited in response to previous CST injury. Patients and methodsWe report a series of six cases of acute ipsilateral weakness or numbness following a hemorrhagic or ischemic stroke from three medical institutions in Saudi Arabia. ResultsThree of these patients presented with right-sided weakness caused by an ipsilateral right hemispheric stroke, while two exhibited left-sided symptoms and one had only left-sided numbness. In all six cases, the ipsilateral corona radiata, internal capsule, basal ganglia, insula, and thalamus were involved. No concomitant opposite hemisphere or brainstem lesion in none of the patients was evident. Two patients had previous strokes affecting the brainstem and left corona radiata, respectively. Complete stroke workup to reveal the cause of stroke was carried out, however no functional MRI was performed. ConclusionIschemic or hemorrhagic stroke may indeed result in ipsilateral weakness or numbness, though in very rare cases. We assume that the most likely mechanism of their ipsilateral weakness subsequent to the ipsilateral stroke was a functional reorganization favoring CST pathways within the ipsilateral hemisphere.

Localizing Delirium through Automated Lesion Segmentation and Neural Network Mapping (N1.001)

<h3>Objective:</h3> To determine whether delirium in acute ischemic stroke is localizable to specific neural networks. <h3>Background:</h3> Delirium is estimated to occur in one-fourth of patients with acute stroke. Despite its associated morbidity and mortality, prediction and pathophysiological understanding of delirium remains challenging. A recent meta-analysis of patients with delirium and stroke found increased risks of delirium in supratentorial, cortical, and anterior circulation strokes, raising the possibility of an underlying neural network for delirium. <h3>Design/Methods:</h3> We performed a retrospective cohort study of patients admitted to a comprehensive stroke center with acute ischemic stroke from January 2016 to April 2019. Patients were assessed for delirium by trained clinical nursing staff using the Confusion Assessment Method (CAM) framework. Acute stroke lesions from MRI diffusion weighted images (DWI) lesions were automatically segmented using a machine learning algorithm. Lesions were registered to a 2mm Montreal Neurological Institute template (MNI-152). We then used lesion network mapping to identify potential unifying brain networks for delirium in patients with acute stroke. <h3>Results:</h3> 907 scans from unique patients were analyzed. 274 patients had delirium (30.2%), 47.5% were women (431), and the mean age was 69.6 years old. In comparison to a general stroke cohort, patients with delirium had lesions connected to the right and left inferior frontal gyri and left middle temporal gyrus and left temporo-parietal junction (one-sample t-test, family-wise error p&lt;0.05). Sensitivity analysis showed that delirium was not associated with parietal, occipital, brainstem, and cerebellar lesions. <h3>Conclusions:</h3> Delirium in stroke localizes to a network connected to frontotemporal regions. These results have implications for prediction of delirium in patients with acute stroke, with the potential for targeting multimodal prevention. Future work will refine their specificity, however, the results suggest that frontotemporal networks may be particularly important for cardinal symptoms of delirium, a disorder of impaired attention and awareness <b>Disclosure:</b> Dr. Rhee has stock in NTAP. Dr. Rhee has stock in TSLA. Dr. Rhee has stock in BABA. Dr. Rhee has stock in ZM. Dr. Rhee has stock in GM. Dr. Rhee has stock in PFF. Dr. Rhee has stock in AMZN. Dr. Rhee has stock in META. Dr. Rhee has stock in GE. Dr. Rhee has received publishing royalties from a publication relating to health care. Dr. Rhee has received personal compensation in the range of $0-$499 for serving as a Director of the Hippocratic Forum with Abigail Adams Institute. Dr. Ferguson has nothing to disclose. Dr. Bonkhoff has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for NeuroImage Clinical (Elsevier). Mr. Patel has nothing to disclose. Dr. Bretzner has nothing to disclose. Dr. Hong has nothing to disclose. Dr. Ryan has nothing to disclose. Dr. Westover has stock in Beacon Biosignals. The institution of Dr. Westover has received research support from NIH. Dr. Westover has received publishing royalties from a publication relating to health care. Dr. Westover has a non-compensated relationship as a cofounder with Beacon Biosignals that is relevant to AAN interests or activities. Dr. Fox has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Wiley. Dr. Rost has received personal compensation in the range of $5,000-$9,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Stroke - AHA/ASA Journal. The institution of Dr. Rost has received research support from NIH. Dr. Rost has received publishing royalties from a publication relating to health care. The institution of Dr. Kimchi has received research support from NIH. The institution of an immediate family member of Dr. Kimchi has received research support from NIH.

Clinical features of patients with MOG-IgG associated disorders and analysis of the relationship between fibrinogen-to-albumin ratio and the severity at disease onset.

The study aimed to investigate the differences in clinical features between pediatric and adult patients with first-episode MOG-IgG associated disorders (MOGAD) and evaluate the relationship between the fibrinogen-to-albumin ratio (FAR) and the severity of neurological deficits at disease onset. We retrospectively collected and analyzed biochemical test results, imaging characteristics, clinical manifestations, expanded disability status scale (EDSS) score, and FAR. The Spearman correlation analysis and logistic regression models were used to examine the association between FAR and severity. Receiver operating characteristic (ROC) curve analysis was to analyze the predictive ability of FAR for the severity of neurological deficits. Fever (50.0%), headache (36.1%), and blurred vision (27.8%) were the most common clinical manifestations in the pediatric group (<18 years old). However, in the adult group (≥18 years old), the most common symptoms were blurred vision (45.7%), paralysis (37.0%), and paresthesia (32.6%). Fever was more common in the pediatric group, while paresthesia was more common in the adult patients, with all differences statistically significant (P < 0.05). The most frequent clinical phenotype in the pediatric group was acute disseminated encephalomyelitis (ADEM; 41.7%), whereas optic neuritis (ON; 32.6%) and transverse myelitis (TM; 26.1%) were more common in the adult group. The differences in clinical phenotype between the two groups were statistically significant (P < 0.05). In both pediatric and adult patients, cortical/subcortical and brainstem lesions were the most common lesions on cranial magnetic resonance imaging (MRI), whereas, for spinal MRI, cervical and thoracic spinal cord lesions were the most commonly observed. According to binary logistic regression analysis, FAR was an independent risk factor for the severity of neurological deficits (odds ratio = 1.717; 95% confidence interval = 1.191-2.477; P = 0.004). FAR (r = 0.359, P = 0.001) was positively correlated with the initial EDSS score. The area under the ROC curve was 0.749. The current study found age-dependent phenotypes in MOGAD patients as ADEM was more commonly observed in patients < 18 years old, while ON and TM were more frequently found in patients ≥18 years old. A high FAR level was an independent indicator for more severe neurological deficits at disease onset in patients with a first episode of MOGAD.

Preliminary exploration of clinical prediction model of severe swallowing disorder after acute ischemic stroke based on nomogram model

To establish a predictive model for severe swallowing disorder after acute ischemic stroke based on nomogram model, and evaluate its effectiveness. A prospective study was conducted. The patients with acute ischemic stroke admitted to Mianyang Central Hospital from October 2018 to October 2021 were enrolled. Patients were divided into severe swallowing disorder group and non-severe swallowing disorder group according to whether severe swallowing disorder occurred within 72 hours after admission. The differences in general information, personal history, past medical history, and clinical characteristics of patients between the two groups were compared. The risk factors of severe swallowing disorder were analyzed by multivariate Logistic regression analysis, and the relevant nomogram model was established. The bootstrap method was used to perform self-sampling internal validation on the model, and consistency index, calibration curve, receiver operator characteristic curve (ROC curve), and decision curve were used to evaluate the predictive performance of the model. A total of 264 patients with acute ischemic stroke were enrolled, and the incidence of severe swallowing disorder within 72 hours after admission was 19.3% (51/264). Compared with the non-severe swallowing disorder group, the severe swallowing disorder group had a higher proportion of patients aged of ≥ 60 years old, with severe neurological deficits [National Institutes of Health stroke scale (NIHSS) score ≥ 7], severe functional impairments [Barthel index, an activity of daily living functional status assessment index, < 40], brainstem infarction and lesions ≥ 40 mm (78.43% vs. 56.81%, 52.94% vs. 28.64%, 39.22% vs. 12.21%, 31.37% vs. 13.62%, 54.90% vs. 24.41%), and the differences were statistically significant (all P < 0.01). Multivariate Logistic regression analysis showed that age ≥ 60 years old [odds ratio (OR) = 3.542, 95% confidence interval (95%CI) was 1.527-8.215], NIHSS score ≥ 7 (OR = 2.741, 95%CI was 1.337-5.619), Barthel index < 40 (OR = 4.517, 95%CI was 2.013-10.136), brain stem infarction (OR = 2.498, 95%CI was 1.078-5.790) and lesion ≥ 40 mm (OR = 2.283, 95%CI was 1.485-3.508) were independent risk factors for severe swallowing disorder after acute ischemic stroke (all P < 0.05). The results of model validation showed that the consistency index was 0.805, and the trend of the calibration curve was basically consistent with the ideal curve, indicating that the model had good prediction accuracy. ROC curve analysis showed that the area under the ROC curve (AUC) predicted by nomogram model for severe swallowing disorder after acute ischemic stroke was 0.817 (95%CI was 0.788-0.852), indicating that the model had good discrimination. The decision curve showed that within the range of 5% to 90%, the nomogram model had a higher net benefit value for predicting the risk of severe swallowing disorder after acute ischemic stroke, indicating that the model had good clinical predictive performance. The independent risk factors of severe swallowing disorder after acute ischemic stroke include age ≥ 60 years old, NIHSS score ≥ 7, Barthel index < 40, brainstem infarction and lesion size ≥ 40 mm. The nomogram model established based on these factors can effectively predict the occurrence of severe swallowing disorder after acute ischemic stroke.

Schwann Cell Remyelination in the Multiple Sclerosis Central Nervous System

Multiple sclerosis (MS) is a central nervous system (CNS) demyelinating disease. Failure to remyelinate successfully is common in MS lesions, often with consequent neuronal/axonal damage. CNS myelin is normally produced by oligodendroglial cells. Remyelination by Schwann cells (SchC) has been reported in spinal cord demyelination, in which SchCs are in close proximity to CNS myelin. We identified an MS cerebral lesion that was remyelinated by SchCs. This prompted us to query the extent of SchC remyelination in the brain and spinal cords of additional autopsied MS specimens. CNS tissues were obtained from the autopsies of 14 MS cases. Remyelinated lesions were identified by Luxol fast blue-periodic-acid Schiff and solochrome cyanine staining. Deparaffinized sections containing remyelinated lesions were stained with anti–glial fibrillary acid protein to identify reactive astrocytes. Glycoprotein P zero (P0) is a protein exclusive to peripheral but not CNS myelin. Areas of SchC remyelination were identified by staining with anti-P0. Myelinated regions in the index case cerebral lesion were confirmed to be of SchC origin using anti-P0 staining. Subsequently, 64 MS lesions from 14 autopsied MS cases were examined, and 23 lesions in 6 cases showed remyelination by SchCs. Lesions from the cerebrum, brainstem, and spinal cord were examined in each case. When present, SchC remyelination was most commonly located adjacent to the venules and associated with a lower surrounding density of glial fibrillary acid protein+ reactive astrocytes than areas of only oligodendroglial cell remyelination. The difference was significant only for spinal cord and brainstem lesions but not for lesions located in the brain. In conclusion, we demonstrated SchC remyelination in the cerebrum, brainstem, and spinal cord of 6 autopsied MS cases. To our knowledge, this is the first report of supratentorial SchC remyelination in MS.

Unilateral erythema in a newborn

A 10-day-old newborn male was referred to our clinic for the evaluation of congenital dermal melanocytosis. During the physical examination, when the baby was lying on his side, a sharply demarcated erythema involving half of his body was noticed (Figure 1). The change of colour lasted a few minutes. The baby was otherwise healthy, and no additional signs were observed. The baby's mother reported only one other isolated similar episode of about the same duration occurring at home when the baby was lying naked on the changing table. HP is a rare event that consists of a sudden unilateral transient change in skin colour with a sharp demarcation along the body midline, resulting in two different body colours.1 HP usually occurs between the 3rd and 4th day of life, and typically appears when the baby is lying on the side and may last from 30 s up to 20 min. It can be a single event or it can be recurrent. Newborns can experience several episodes in just a few days.2 Pathophysiology of HP is still not completely clear although there is evidence to support a sympathetic autonomic dysfunction, probably because of hypothalamic immaturity in the newborn.2 HP represents a benign condition although it has also been reported in the context of hypoxia and as an epiphenomenon of central nervous system disorders such as meningitis, hypothalamic and brain stem lesions or sympathetic nervous system lesions. Exacerbation has been described in patients receiving treatment with prostaglandin E1.1, 3 While the clinical characteristics of HP make it easily distinguishable, a differential diagnosis should include infectious neonatal skin rashes, such as parechovirus, herpes virus and candida infection, neonatal lupus erythematosus and capillary malformations such as those in the PROS spectrum and cutis marmorata telangiectatica congenita. HP can be a manifestation of the rare disorder paroxysmal extreme pain disorder, part of SCN9A neuropathic pain syndromes, a group of sodium channelopathies where systemic symptoms such as tonic nonepileptic attacks and syncope with bradycardia are associated with the transient skin colour change.4 HP is a benign and self-resolving phenomenon. As mentioned, only in rare circumstances HP is a manifestation of central nervous system disorders in association with other signs and symptoms and never presenting as the sole clue of such conditions.5 The recognition of the phenomenon is therefore important since, while being certainly peculiar, it does not require further investigations or therapeutic measures. Alice Nadia Rossi wrote the first draft of the manuscript and adjusted it according to the comments of the other authors. Francesco Paolo Salamone collected data and clinical images and helped writing the manuscript. Martina Mussi participated in data collection. Marco Adriano Chessa participated in the revision of the manuscript. Iria Neri carried out the final revision of the manuscript before submission. All of the authors participated in the preparation of the manuscript. There are no prior publications or submissions with any overlapping information, including studies and patients. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. The authors declare no conflicts of interest. All patients in this manuscript have given written informed consent for participation in the study and the use of their de-identified, anonymized, aggregated data and their case details (including photographs) for publication. Data sharing is not applicable to this article as no new data were created or analysed in this study.

Where art thou? Reflecting on auditory hallucinosis

IntroductionHallucinosis has evolved out of classification systems but what about patients who present with exclusive or almost exclusive hallucinations? Auditory hallucinations are especially likely to swiftly be considered due to psychiatric illness.An elderly patient with chronic auditory hallucinations without other significant psychopathology nor other symptoms prompted reflection and literature review.ObjectivesTo review differential diagnosis of auditory hallucinosis.MethodsPubmed search for terms: auditory and hallucinosis.ResultsHallucinations should be evaluated according to: type, onset and evolution, association with physical and /or neurological symptoms, association with other hallucinations and/or other psychopathology, characteristics.Auditory hallucinations may present along a continuum from tinnitus, simple, verbal, musical.The Pubmed search retrieved articles pertaining to auditory hallucinations associated with:1. Sensory deprivation; 2. Hearing loss, auditory Charles Bonnet syndrome; 3. Dementia, neurodegenerative disorders; 4. Brainstem lesions; 5. Other central nervous lesions: thalamus, temporal, other; 6. Epilepsy; 7. Tic disorders; 8. Alcohol use disorders; 9. Borderline personality disorder; 10. Others.ConclusionsPatients presenting with auditory hallucinosis should be carefully evaluated to exclude non-psychiatric disorders.In some patients, such as the one who prompted the review, an identifiable cause may not yet be found.Disclosure of InterestNone Declared

Clinical Findings in a Pati ent with Large B-Cell Lymphoma andNeuroniti s: A Case Study.

Given the multifaceted nature of the balance system, an interdisciplinary approach to patient care is imperative. For surgical patients with complex medical histories, comprehensive vestibular evaluations provide information on baseline vestibular function and identify possible surgical risks and outcomes. This case study follows a patient diagnosed with probable right vestibular neuronitis immediately preceding surgical resection of a left brainstem lesion, later diagnosed as a B cell lymphoma (BCL) and provides details regarding pre- and postsurgical outcomes. This case study expands on the importance of the inclusion of vestibular audiologists on the interdisciplinary team for related surgical procedures to provide insight into possible surgical risks and subsequent effects on patients' postsurgical quality of life. Case report. A 68-year-old female patient evaluated within the Henry Ford Health System for management of diffuse large BCL. Standard neuro-otology, neuro-surgical, audiological, and vestibular evaluations were conducted to evaluate the patient's complex symptomology. This case report outlines a patient hospitalized for a left brainstem mass, later diagnosed as an aggressive form of lymphoma, with a concurrent episode of vestibular neuronitis on the contralesional side. Functional outcomes are discussed following surgical intervention to remove the mass. Postsurgical vestibular testing revealed a bilateral vestibular hypofunction. Vestibular audiology plays an essential role in the multidisciplinary team for complex dizzy patients with related surgical procedures, as this subset of the field can offer critical insight into postsurgical recommendations and patient expectations.

Body Lateropulsion and Pusher Behavior

The relationship between postural disturbance and vertical perception after cerebrovascular disease remains unclear and studies have only recently begun to be conducted. On the other hand, the symptomatic aspect is evident: body lateropulsion is ipsilateral in the case of caudal brainstem lesions and contralateral in the case of rostral brainstem and cerebral hemispheric lesions. In addition, patients with cerebral hemispheric lesions sometimes show“pusher behavior” in which they resist any attempt to correct their posture and push the body back to the paralyzed side using the healthy limbs, as they have a fear of deviation to the healthy side. The pusher behavior is always accompanied by hemiplegia and is detected in about 10% of cases of hemispheric vascular lesions.