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Neuropeptide S (NPS) was postulated to be a wake-promoting neuropeptide with unknown mechanism, and a mutation in its receptor (NPSR1) causes the short sleep duration trait in humans. We investigated the role of different NPS+ nuclei in sleep/wake regulation. Loss-of-function and chemogenetic studies revealed that NPS+ neurons in the parabrachial nucleus (PB) are wake-promoting, whereas peri-locus coeruleus (peri-LC) NPS+ neurons are not important for sleep/wake modulation. Further, we found that a NPS+ nucleus in the central gray of the pons (CGPn) strongly promotes sleep. Fiber photometry recordings showed that NPS+ neurons are wake-active in the CGPn and wake/REM-sleep active in the PB and peri-LC. Blocking NPS-NPSR1 signaling or knockdown of Nps supported the function of the NPS-NPSR1 pathway in sleep/wake regulation. Together, these results reveal that NPS and NPS+ neurons play dichotomous roles in sleep/wake regulation at both the molecular and circuit levels.

Sleeping animals can be woken up rapidly by external threat signals, which is an essential defense mechanism for survival. However, neuronal circuits underlying the fast transmission of sensory signals for this process remain unclear. Here, we report in mice that alerting sound can induce rapid awakening within hundreds of milliseconds and that glutamatergic neurons in the pontine central gray (PCG) play an important role in this process. These neurons exhibit higher sensitivity to auditory stimuli in sleep than wakefulness. Suppressing these neurons results in reduced sound-induced awakening and increased sleep in intrinsic sleep/wake cycles, whereas their activation induces ultra-fast awakening from sleep and accelerates awakening from anesthesia. Additionally, the sound-induced awakening can be attributed to the propagation of auditory signals from the PCG to multiple arousal-related regions, including the mediodorsal thalamus, lateral hypothalamus, and ventral tegmental area. Thus, the PCG serves as an essential distribution center to orchestrate a global auditory network to promote rapid awakening. [Display omitted] • PCG glutamatergic neurons contribute to sound-induced rapid awakening • They exhibit higher sensitivity in sleep and modulate intrinsic sleep/wake states • Their activation induces ultra-fast awakening from NREM sleep • PCG transmits auditory signals to a multitude of arousal-related brain regions The ability to rapidly wake up from sleep upon threat signals is critical for animal survival. In this study, Wei et al. report that the pontine central gray (PCG) is a critical node of a fast-execution alerting system and globally broadcasts alerting auditory signals to a distributed brain network to promote awakening. [ABSTRACT FROM AUTHOR]

Considering that the retrotrapezoid nucleus/respiratory parafacial region (RTN/pFRG) would be an important center in the central nervous system involved in the maintenance and modulation of respiratory activity, we hypothesized that neurons in this nucleus would also be involved in the postinspiratory (post-I) phase of the respiratory cycle through a connection with the pontine Kölliker-Fuse (KF) region. Here, we performed pharmacogenetic manipulation (AAV-hM3D(Gq)-mCherry or AAV-hM4D(Gi)-mCherry) in VGlut2-cre, Ai6 conscious mice to evaluate breathing parameters through whole body plethysmography under baseline conditions (normoxia: F I O 2 = 0.21) or under hypercapnia or hypoxia challenges (F I C O 2 = 0.07 or F I O 2 = 0.08). Under normoxia, selective stimulation of RTN/pFRG resulted in a smaller increase in V̇ e (1,272 ± 102.5, vs. RTN/pFRG stimulation: 1,878 ± 122.1 mL/kg/min), due to a smaller increase in VT (5.4 ± 0.35, vs. RTN/pFRG stimulation: 7.77 ± 0.21 mL/kg) without changing fR in a condition of KF inhibition. However, inhibition of the VGlut2 neurons in the KF did affect the TE1 produced by selective activation of RTN/pFRG (119.9 ± 2.53, vs. RTN/pFRG stimulation: 104 ± 2.46 ms). Both the hypercapnia and hypoxia ventilatory response were reduced after inhibition of VGlut2-expressing KF neurons. Therefore, consistent with anatomical projections RTN/pFRG neurons regulate lung ventilation by controlling all aspects of breathing, i.e., breathing frequency, inspiration, postinspiration, and active expiration. All the modulation seems to be dependent on the integrity of the glutamatergic neurons in the KF region. NEW & NOTEWORTHY: Our research reveals specific roles and interactions between the retrotrapezoid nucleus/respiratory parafacial region (RTN/pFRG) and the pontine Kölliker-Fuse (KF) region in controlling respiratory phases. RTN/pFRG neurons are key in regulating all aspects of breathing, including frequency, inspiration, postinspiration, and active expiration. This regulation depends on the functional integrity of glutamatergic neurons in the KF region, aligning with anatomical projections. [ABSTRACT FROM AUTHOR]

Objective To investigate whether focal demyelination in the pontine trigeminal tracts (PTTs) can induce trigeminal neuralgia-like behaviors in adult rats. Methods Brain stereotaxic microinjection technology was used to inject 1% lysophosphatidylcholine (LPC) or 1× PBS into the PTT region of male SD rats (weighing 250~270 g) to establish the PTT demyelination model group (LPC group) and control group, respectively. Myelin fluorescent staining was employed to evaluate the demyelination changes in the PTT region. Behavioral experiments were performed to measure the mechanical stimulation threshold of head withdraw response, unilateral eyelid contraction duration and numbers of fast face stroking in rats. Intraperitoneal injection of 50 mg/kg carbamazepine was given to the rats to evaluate their behavioral changes. Results A stable local demyelination model of PTT in adult rats was successfully established by, with the coordinate origin at Bregma, descending glass microelectrode for 9.22 mm with a left-side 18° tilt path from axterior-posterior (AP) -9.86 mm, medial-lateral (ML) 0 mm and dorsal-ventral (DV) 0 mm, and then 250 nL 1%LPC was injected at a rate of 250 nL/min. Myelin fluorescent staining demonstrated that the peak of demyelination was observed at the 7th day after modeling. Behavioral experiments showed that compared with the control group, the air-puff gas stimulation threshold and von Frey filament stimulation threshold that triggered the head withdraw response were significantly reduced in the LPC group (P < 0.01). At the 7th day after modeling, there were significant increases in the unilateral eyelid contraction duration and the numbers of unilateral fast face stroking only in the adult rats from the LPC groups (P < 0.01). Carbamazepine significantly decreased the numbers of unilateral fast face stroking evoked by mechanical stimulation (P < 0.01). Conclusion Focal demyelination in the PTTs can induce trigeminal neuralgia-like behaviors in adult rats.

Background: An accumulating body of research indicates that the pons is related to the occurrence of depression. Si-Ni-San (SNS) is a well-known Chinese herbal formula that is used to treat depression. Chinese herbal formulae have multiple therapeutic characteristics. Although it has been proven that SNS can exert antidepressant effects by improving changes in the limbic system, it is currently unclear whether SNS has therapeutic targets in the pons. This study aimed to explore the therapeutic targets of SNS in the pons for depression treatment. Materials and methods: Two experiments were conducted. In Experiment 1, 32 rats were divided into four groups: (1) a Control (C) group that received distilled water as a vehicle; (2) a Model (M) group that received the chronic unpredictable mild stress (CUMS) procedure and was administered distilled water; (3) a Stress + SNS (MS) group that received the CUMS procedure and was administered SNS dissolved in distilled water; and (4) a Stress + Fluoxetine (MF) group that received the CUMS procedure and was administered fluoxetine dissolved in distilled water. The open field test (OFT), the sucrose preference test (SPT), and the novel object recognition test (NOR) were performed to test the antidepressant effects of SNS. High-throughput mRNA sequencing (RNA-seq) was used to explore possible gene targets of SNS in the pons, and quantitative real-time PCR was performed to verify the results. High-performance liquid chromatography was used to detect neurotransmitters. Finally, correlation analyses were conducted between behaviors, genes expression, and neurotransmitters. In Experiment 2, 18 rats were divided into the same three groups as in Experiment 1: (1) C, (2) M, and (3) MS. fMRI was used to confirm whether SNS altered the pons in a rat model of depression. Results: SNS significantly improved sucrose preference in the SPT and TN-TO in the NOR compared to the M group (P < 0.05). RNA-seq filtered 49 differentially expressed genes(DEGs) that SNS could reverse in the pons of the CUMS depression model. Real-time PCR detected six genes, including Complexin2 (Cplx2), Serpinf1, Neuregulin1 (Nrg1), Annexin A1 (Anxa1), β-arrestin 1 (Arrb1) and presenilin 1 (Psen1). SNS significantly reversed changes in the expression of Anxa1, Nrg1, and Psen1 caused by CUMS (P < 0.05), which is consistent with the DEGs results. Additionally, SNS significantly reversed norepinephrine (NE) changes in the pons. There were 18 noteworthy correlations between behavior, genes, and neurotransmitters (P < 0.05). fMRI showed that SNS can decrease the amplitude of low-frequency fluctuations (ALFF) in the pons of living depressed rats. Conclusion: The pons is an important target brain region for SNS to exert its antidepressant effects. SNS may improve pontine NE levels by regulating the Anxa1, Nrg1, and Psen1 genes, thereby exerting antidepressant effects and improving cognitive function. [ABSTRACT FROM AUTHOR]

Introduction: Recurrent isolated sleep paralysis (RISP) is a rapid eye movement sleep (REM) parasomnia, characterized by the loss of voluntary movements upon sleep onset and/or awakening with preserved consciousness. Evidence suggests microstructural changes of sleep in RISP, although the mechanism of this difference has not been clarified yet. Our research aims to identify potential morphological changes in the brain that can reflect these regulations. Materials and methods: We recruited 10 participants with RISP (8 women; mean age 24.7 years; SD 2.4) and 10 healthy control subjects (w/o RISP; 3 women; mean age 26.3 years; SD 3.7). They underwent video-polysomnography (vPSG) and sleep macrostructure was analyzed. After that participants underwent magnetic resonance imaging (MRI) of the brain. We focused on 2-dimensional measurements of cerebellum, pons and thalamus. Statistical analysis was done in SPSS program. After analysis for normality we performed Mann-Whitney U test to compare our data. Results: We did not find any statistically significant difference in sleep macrostructure between patients with and w/o RISP. No evidence of other sleep disturbances was found. 2-dimensional MRI measurements revealed statistically significant increase in cerebellar vermis height (p = 0.044) and antero-posterior diameter of midbrain-pons junction (p = 0.018) in RISP compared to w/o RISP. Discussion: Our results suggest increase in size of cerebellum and midbrainpons junction in RISP. This enlargement could be a sign of an over-compensatory mechanism to otherwise dysfunctional regulatory pathways. Further research should be done to measure these differences in time and with closer respect to the frequency of RISP episodes. [ABSTRACT FROM AUTHOR]

Chronic intermittent hypoxia (CIH) is a prevalent condition characterized by recurrent episodes of oxygen deprivation, linked to respiratory and neurological disorders. Prolonged CIH is known to have adverse effects, including endothelial dysfunction, chronic inflammation, oxidative stress, and impaired neuronal function. These factors can contribute to serious comorbidities, including metabolic disorders and cardiovascular diseases. To investigate the molecular impact of CIH, we examined male C57BL/6J mice exposed to CIH for 21 days, comparing with normoxic controls. We used single-nucleus RNA sequencing to comprehensively examine the transcriptomic impact of CIH on key cell classes within the brainstem, specifically excitatory neurons, inhibitory neurons, and oligodendrocytes. These cell classes regulate essential physiological functions, including autonomic tone, cardiovascular control, and respiration. Through analysis of 10,995 nuclei isolated from pontine-medullary tissue, we identified seven major cell classes, further subdivided into 24 clusters. Our findings among these cell classes, revealed significant differential gene expression, underscoring their distinct responses to CIH. Notably, neurons exhibited transcriptional dysregulation of genes associated with synaptic transmission, and structural remodeling. In addition, we found dysregulated genes encoding ion channels and inflammatory response. Concurrently, oligodendrocytes exhibited dysregulated genes associated with oxidative phosphorylation and oxidative stress. Utilizing CellChat network analysis, we uncovered CIH-dependent altered patterns of diffusible intercellular signaling. These insights offer a comprehensive transcriptomic cellular atlas of the pons-medulla and provide a fundamental resource for the analysis of molecular adaptations triggered by CIH. NEW & NOTEWORTHY This study on chronic intermittent hypoxia (CIH) from pons-medulla provides initial insights into the molecular effects on excitatory neurons, inhibitory neurons, and oligodendrocytes, highlighting our unbiased approach, in comparison with earlier studies focusing on single target genes. Our findings reveal that CIH affects cell classes distinctly, and the dysregulated genes in distinct cell classes are associated with synaptic transmission, ion channels, inflammation, oxidative stress, and intercellular signaling, advancing our understanding of CIH-induced molecular responses. [ABSTRACT FROM AUTHOR]

Diffuse pontine glioblastoma multiforme is a rare subtype of glioblastoma associated with a poor prognosis. In this case report, we present a unique case of diffuse primary pontine glioblastoma multiforme in a patient without any supratentorial lesions. We review the symptoms, treatment options, and case management of patients with infratentorial glioblastoma multiforme and compare these with our patient. Our patient presented with symptoms including progressive diplopia, gait disturbance, and lower extremity weakness. Magnetic resonance imaging revealed a diffuse lesion involving the pons and biopsy revealed only mildly-atypical glial infiltrates. Consequentially, diagnosis was driven by genetic analysis. Due to the location of the tumor, surgery was not considered a viable option. Instead, the patient received radiation therapy along with concomitant and adjuvant temozolomide chemotherapy which has resulted in improvement of symptoms. This case highlights the challenges of managing diffuse primary pontine glioblastoma multiforme and the need for more effective treatment options for this rare subtype of glioblastoma. Despite aggressive treatment, the prognosis for patients with infratentorial glioblastoma multiforme remains poor, with a median survival time of less than a year. Further research is needed to improve our understanding of the biology and optimal management of this disease. [ABSTRACT FROM AUTHOR]

IntroductionRecurrent isolated sleep paralysis (RISP) is a rapid eye movement sleep (REM) parasomnia, characterized by the loss of voluntary movements upon sleep onset and/or awakening with preserved consciousness. Evidence suggests microstructural changes of sleep in RISP, although the mechanism of this difference has not been clarified yet. Our research aims to identify potential morphological changes in the brain that can reflect these regulations.Materials and methodsWe recruited 10 participants with RISP (8 women; mean age 24.7 years; SD 2.4) and 10 healthy control subjects (w/o RISP; 3 women; mean age 26.3 years; SD 3.7). They underwent video-polysomnography (vPSG) and sleep macrostructure was analyzed. After that participants underwent magnetic resonance imaging (MRI) of the brain. We focused on 2-dimensional measurements of cerebellum, pons and thalamus. Statistical analysis was done in SPSS program. After analysis for normality we performed Mann–Whitney U test to compare our data.ResultsWe did not find any statistically significant difference in sleep macrostructure between patients with and w/o RISP. No evidence of other sleep disturbances was found. 2-dimensional MRI measurements revealed statistically significant increase in cerebellar vermis height (p = 0.044) and antero-posterior diameter of midbrain-pons junction (p = 0.018) in RISP compared to w/o RISP.DiscussionOur results suggest increase in size of cerebellum and midbrain-pons junction in RISP. This enlargement could be a sign of an over-compensatory mechanism to otherwise dysfunctional regulatory pathways. Further research should be done to measure these differences in time and with closer respect to the frequency of RISP episodes.

A shared mechanism across species heralds the arrival of self-generated sensations, helping the brain to anticipate, and therefore distinguish, self-generated from externally generated sensations. In mammals, this sensory prediction mechanism is supported by communication within a cortico-ponto-cerebellar-thalamo-cortical loop. Schizophrenia is associated with impaired sensory prediction as well as abnormal structural and functional connections between nodes in this circuit. Despite the pons principal role in relaying and processing sensory information passed from the cortex to cerebellum, few studies have examined pons connectivity in schizophrenia. Here, we first briefly describe how the pons contributes to sensory prediction. We then summarize schizophrenia-related abnormalities in the cortico-ponto-cerebellar-thalamo-cortical loop, emphasizing the dearth of research on the pons relative to thalamic and cerebellar connections. We conclude with recommendations for advancing our understanding of how the pons relates to sensory prediction failures in schizophrenia.

Background: Various MRI markers—including midbrain and pons areas (Marea, Parea) and volumes (Mvol, Pvol), ratios (M/Parea, M/Pvol), and composite markers (magnetic resonance imaging Parkinsonism Indices 1,2; MRPI 1,2)—have been proposed as imaging markers of Richardson's syndrome (RS) and multiple system atrophy–Parkinsonism (MSA-P). A systematic review/meta-analysis of relevant studies aiming to compare the diagnostic accuracy of these imaging markers is lacking. Methods: Pubmed and Scopus were searched for studies with >10 patients (RS, MSA-P or CBS) and >10 controls with data on Marea, Parea, Mvol, Pvol, M/Parea, M/Pvol, MRPI 1, and MRPI 2. Cohen's d, as a measure of effect size, was calculated for all markers in RS, MSA-P, and CBS. Results: Twenty-five studies on RS, five studies on MSA-P, and four studies on CBS were included. Midbrain area provided the greatest effect size for differentiating RS from controls (Cohen's d = −3.10; p < 0.001), followed by M/Parea and MRPI 1. MSA-P had decreased midbrain and pontine areas. Included studies exhibited high heterogeneity, whereas publication bias was low. Conclusions: Midbrain area is the optimal MRI marker for RS, and pons area is optimal for MSA-P. M/Parea and MRPIs produce smaller effect sizes for differentiating RS from controls. [ABSTRACT FROM AUTHOR]

The brainstem pedunculopontine (PPN) and laterodorsal tegmental (LDTg) nuclei are involved in multifarious activities, including motor control. Yet, their exact cytoarchitectural boundaries are still uncertain. We therefore initiated a comparative study of the topographical and neurochemical organization of the PPN and LDTg in cynomolgus monkeys (Macaca fascicularis) and humans. The distribution and morphological characteristics of neurons expressing choline acetyltransferase (ChAT) and/or nicotinamide adenine dinucleotide phosphate diaphorase (Nadph‐δ) were documented. The number and density of the labeled neurons were obtained by stringent stereological methods, whereas their topographical distribution was reported upon corresponding magnetic resonance imaging (MRI) planes. In both human and nonhuman primates, the PPN and LDTg are populated by three neurochemically distinct types of neurons (ChAT‐/Nadph‐δ+, ChAT+/Nadph‐δ‐, and ChAT+/Nadph‐δ+), which are distributed according to a complex spatial interplay. Three‐dimensional reconstructions reveal that ChAT+ neurons in the PPN and LDTg form a continuum with some overlaps with pigmented neurons of the locus coeruleus, dorsally, and of the substantia nigra (SN) complex, ventrally. The ChAT+ neurons in the PPN and LDTg are —two to three times more numerous in humans than in monkeys but their density is —three to five times higher in monkeys than in humans. Neurons expressing both ChAT and Nadph‐δ have a larger cell body and a longer primary dendritic arbor than singly labeled neurons. Stereological quantification reveals that 25.6% of ChAT+ neurons in the monkey PPN are devoid of Nadph‐δ staining, a finding that questions the reliability of Nadph‐δ as a marker for cholinergic neurons in primate brainstem. [ABSTRACT FROM AUTHOR]

Birds have a comprehensive network of sensorimotor projections extending from the forebrain and midbrain to the cerebellum via the pontine nuclei, but the organization of these circuits in the pons is not thoroughly described. Inputs to the pontine nuclei include two retinorecipient areas, nucleus lentiformis mesencephali (LM) and nucleus of the basal optic root (nBOR), which are important structures for analyzing optic flow. Other crucial regions for visuomotor control include the retinorecipient ventral lateral geniculate nucleus (GLv), and optic tectum (TeO). These visual areas, together with the somatosensory area of the anterior (rostral) Wulst, which is homologous to the primary somatosensory cortex in mammals, project to the medial and lateral pontine nuclei (PM, PL). In this study, we used injections of fluorescent tracers to study the organization of these visual and somatosensory inputs to the pontine nuclei in zebra finches. We found a topographic organization of inputs to PM and PL. The PM has a lateral subdivision that predominantly receives projections from the ipsilateral anterior Wulst. The medial PM receives bands of inputs from the ipsilateral GLv and the nucleus laminaris precommisulis, located medial to LM. We also found that the lateral PL receives a strong ipsilateral projection from TeO, while the medial PL and region between the PM and PL receive less prominent projections from nBOR, bilaterally. We discuss these results in the context of the organization of pontine inputs to the cerebellum and possible functional implications of diverse somato‐motor and visuomotor inputs and parcellation in the pontine nuclei. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Normal aging results in brainstem atrophy. In making diagnosis of Progressive Supranuclear Palsy (PSP) and other Parkinson s s disease spectrums, midbrain-pons ratio has been utilized as a radiological indicator. AIM: To estimate the ratio and size of the midbrain and pons areas in the adult and elderly populations of Pakistan. This is because no study is available till date. MATERIALS AND METHODS: This cross-sectional, analytical study was done in Shifa International Hospital, Islamabad, Pakistan, from January 2023 to March 2023 in which midbrain area and pons area was calculated and their ratio were taken with respect to age an gender. RESULTS: Reduction in midbrain to pons ratio was seen with increasing age, normal aging process. CONCLUSION: When evaluating the findings, age must be considered because the midbrain to pons area ratio decreases considerably with age. [ABSTRACT FROM AUTHOR]

The rhombicbrain (rhombencephalon or intermediate sector) is the vertebrate central nervous system part between the forebrain-midbrain (rostral sector) and spinal cord (caudal sector), and it has three main divisions: pons, cerebellum, and medulla. Using a data-driven approach, here we examine intrinsic rhombicbrain (intrarhombicbrain) network architecture that in rat consists of 52,670 possible axonal connections between 230 gray matter regions (115 bilaterally symmetrical pairs). Our analysis indicates that only 8,089 (15.4%) of these connections exist. Multiresolution consensus cluster analysis yields a nested hierarchy model of rhombicbrain subsystems that at the top level are associated with 1) the cerebellum and vestibular nuclei, 2) orofacial-pharyngeal-visceral integration, and 3) auditory connections; the bottom level has 68 clusters, ranging in size from 2 to 11 regions. The model provides a basis for functional hypothesis development and interrogation. More granular network analyses performed on the intrinsic connectivity of individual and combined main rhombicbrain divisions (pons, cerebellum, medulla, pons + cerebellum, and pons + medulla) demonstrate the mutability of network architecture in response to the addition or subtraction of connections. Clear differences between the structure-function network architecture of the rhombicbrain and forebrain-midbrain are discussed, with a stark comparison provided by the subsystem and small-world organization of the cerebellar cortex and cerebral cortex. Future analysis of the connections within and between the forebrain-midbrain and rhombicbrain will provide a model of brain neural network architecture in a mammal. [ABSTRACT FROM AUTHOR]

MED27 is a subunit of the Mediator multiprotein complex, which is involved in transcriptional regulation. Biallelic MED27 variants have recently been suggested to be responsible for an autosomal recessive neurodevelopmental disorder with spasticity, cataracts and cerebellar hypoplasia. We further delineate the clinical phenotype of MED27 -related disease by characterizing the clinical and radiological features of 57 affected individuals from 30 unrelated families with biallelic MED27 variants. Using exome sequencing and extensive international genetic data sharing, 39 unpublished affected individuals from 18 independent families with biallelic missense variants in MED27 have been identified (29 females, mean age at last follow-up 17 ± 12.4 years, range 0.1–45). Follow-up and hitherto unreported clinical features were obtained from the published 12 families. Brain MRI scans from 34 cases were reviewed. MED27 -related disease manifests as a broad phenotypic continuum ranging from developmental and epileptic-dyskinetic encephalopathy to variable neurodevelopmental disorder with movement abnormalities. It is characterized by mild to profound global developmental delay/intellectual disability (100%), bilateral cataracts (89%), infantile hypotonia (74%), microcephaly (62%), gait ataxia (63%), dystonia (61%), variably combined with epilepsy (50%), limb spasticity (51%), facial dysmorphism (38%) and death before reaching adulthood (16%). Brain MRI revealed cerebellar atrophy (100%), white matter volume loss (76.4%), pontine hypoplasia (47.2%) and basal ganglia atrophy with signal alterations (44.4%). Previously unreported 39 affected individuals had seven homozygous pathogenic missense MED27 variants, five of which were recurrent. An emerging genotype-phenotype correlation was observed. This study provides a comprehensive clinical-radiological description of MED27 -related disease, establishes genotype-phenotype and clinical-radiological correlations and suggests a differential diagnosis with syndromes of cerebello-lental neurodegeneration and other subtypes of 'neuro-MEDopathies'. [ABSTRACT FROM AUTHOR]

Rett syndrome (RTT) is a severe neurodevelopmental disorder that mainly affects females due to silencing mutations in the X-linked MECP2 gene. One of the most troubling symptoms of RTT is breathing irregularity, including apneas, breath-holds, and hyperventilation. Mice with silencing mutations in Mecp2 exhibit breathing abnormalities similar to human patients and serve as useful models for studying mechanisms underlying breathing problems in RTT. Previous work implicated the pontine, respiratory-controlling Kölliker-Fuse (KF) in the breathing problems in RTT. The goal of this study was to test the hypothesis that inhibitory synaptic transmission is deficient in KF neurons from symptomatic male and female RTT mice. We performed whole cell voltage-clamp recordings from KF neurons in acute brain slices to examine spontaneous and electrically evoked inhibitory post-synaptic currents (IPSCs) in RTT mice and age- and sex-matched wild-type mice. The frequency of spontaneous IPSCs was reduced in KF neurons from male RTT mice but surprisingly not in female RTT mice. In addition, electrically evoked IPSCs were less reliable in KF neurons from male, but not female, RTT mice, which was positively correlated with paired-pulse facilitation, indicating decreased probability of release. KF neurons from male RTT mice were also more excitable and exhibited shorter-duration action potentials. Increased excitability of KF neurons from male mice was not explained by changes in axon initial segment length. These findings indicate impaired inhibitory neurotransmission and increased excitability of KF neurons in male but not female RTT mice and suggest that sex-dependent mechanisms contribute to breathing problems in RTT. NEW & NOTEWORTHY Kölliker-Fuse (KF) neurons in acute brain slices from male Rett syndrome (RTT) mice receive reduced inhibitory synaptic inputs compared with wild-type littermates. In female RTT mice, inhibitory transmission was not different in KF neurons compared with controls. The results from this study show that sex-specific alterations in synaptic transmission occur in the KF of RTT mice. [ABSTRACT FROM AUTHOR]

Diffuse pontine glioblastoma multiforme is a rare subtype of glioblastoma associated with a poor prognosis. In this case report, we present a unique case of diffuse primary pontine glioblastoma multiforme in a patient without any supratentorial lesions. We review the symptoms, treatment options, and case management of patients with infratentorial glioblastoma multiforme and compare these with our patient. Our patient presented with symptoms including progressive diplopia, gait disturbance, and lower extremity weakness. Magnetic resonance imaging revealed a diffuse lesion involving the pons and biopsy revealed only mildly-atypical glial infiltrates. Consequentially, diagnosis was driven by genetic analysis. Due to the location of the tumor, surgery was not considered a viable option. Instead, the patient received radiation therapy along with concomitant and adjuvant temozolomide chemotherapy which has resulted in improvement of symptoms. This case highlights the challenges of managing diffuse primary pontine glioblastoma multiforme and the need for more effective treatment options for this rare subtype of glioblastoma. Despite aggressive treatment, the prognosis for patients with infratentorial glioblastoma multiforme remains poor, with a median survival time of less than a year. Further research is needed to improve our understanding of the biology and optimal management of this disease.

Pontine autosomal dominant microangiopathy and leukoencephalopathy (PADMAL) is a rare hereditary cerebral small vessel disease. We report a novel collagen type IV alpha 1 (COL4A1) gene mutation in a Chinese family with PADMAL. The index case was followed up for 6 years. Neuroimaging, whole-exome sequencing, skin biopsy, and pedigree analysis were performed. She initially presented with minor head injury at age 38. MRI brain showed chronic lacunar infarcts in the pons, left thalamus, and right centrum semiovale. Extensive workup was unremarkable except for a patent foramen ovale (PFO). Despite anticoagulation, PFO closure, and antiplatelet therapy, the patient had recurrent lacunar infarcts in the pons and deep white matter, as well as subcortical microhemorrhages. Whole-exome sequencing demonstrated a novel c.*34G > T mutation in the 3' untranslated region of COL4A1 gene. Skin biopsy subsequently demonstrated thickening of vascular basement membrane, proliferation of endothelial cells, and stenosis of vascular lumen. Three additional family members had gene testing and 2 of them were found to have the same heterozygous mutation. Of the 18 individuals in the pedigree of 3 generations, 12 had clinical and MRI evidence of PADMAL. The mechanisms of both ischemic and hemorrhagic stroke are likely the overexpression of COLT4A1 in the basement membrane and frugality of the vessel walls. Our findings suggest that the novel c.*34G > T mutation appears to have the same functional consequences as the previously reported COL4A1 gene mutations in patients with PADMAL and multi-infarct dementia of Swedish type.

Objective ‒ to sharpen the attention of doctors to a rare, little-known pathology of damage to the ventral parts of the pons, the upper parts of the medulla oblongata ‒ the locked-in syndrome. The extremely important value of this syndrome can be in determining the prognosis of the disease and solving issues of rehabilitation and patient care. Locked-in syndrome is a rare, complex clinical and neurological symptom complex, the basis of which is a lesion of the front parts of the pons with intact functioning of the nuclei and afferents of the brain stem cover. The locked-in syndrome occurs when blood circulation is disturbed in the ventral parts of the brain stem and pons. According to the criteria of the American Congress of Rehabilitation Medicine, the locked-in syndrome is a combination of: 1) stable opening of the eyes; 2) safety of basic cognitive abilities; 3) aphonia or severe hypophonia; 4) tetraplegia or tetraparesis; 5) the main method of communication, used by the patient – movement of the eyes in a vertical or horizontal plane or blinking of the upper eyelid. The definition of this syndrome and the localization of its injuries, which cause it, became possible when long-term lung ventilation and neuroimaging methods ‒ spiral computer tomography and magnetic resonance imaging ‒ were introduced into clinical practice. Three personal observations of the occurrence of the locked-in syndrome of different etiology are given: with ischemic damage to the ventral parts of the pons of the brain, with hemorrhage in the ventral parts of the pons, with traumatic damage to the ventral parts of the brain stem. The dynamics of neurological disorders, their adequate assessment during neuroimaging allow timely diagnosis of the localization of the process and the prognosis of the disease, and therefore the choice of methods of treatment, rehabilitation or long-term care for the patient.

Posterior circulation stroke is an uncommon cause of sudden-onset sensorineural hearing loss (SSNHL). Anterior inferior cerebellar artery occlusion results in ipsilateral peripheral audiovestibular dysfunction. Few reports describe posterior circulation stroke presenting with contralateral SSNHL and acute vestibular and focal neurological signs. We present a case of contralateral SSNHL and isolated acute central vestibular dysfunction in the absence of other central focal neurological deficits. To the best of our knowledge, this has not been described to date. The patient was identified to have asymmetrical SSNHL, subtle skew deviation with left head tilt, and significant refixation saccades on video head impulse test despite bilaterally normal vestibulo-ocular reflex gains. Left pontine infarct was suspected and confirmed on magnetic resonance imaging. The patient was treated with an appropriate antiplatelet regimen. We highlight the importance of a thorough clinical diagnostic work-up as posterior circulation strokes with isolated audiovestibular deficits can be easily missed if other significant neurological deficits are absent.

We present a rare neurosurgical entity in a 9-year-old girl who presented with a three-day history of right-sided weakness and numbness. Her parents reported hospitalization six years ago with similar symptoms, due to a probable brainstem cavernous malformation. At that time, she underwent excision of a cortical lesion (probable cavernoma) and conservative management of the brainstem lesion with dexamethasone. Her brain magnetic resonance imaging scan in our hospital revealed a large cavernous malformation protruding into the 4th ventricle, with recent bleeding and mass effect to the pons, as well as another hypothalamic cavernoma. She was conservatively managed with intravenous dexamethasone and discharged home three days later with no deficits, on a tapering scheme of oral dexamethasone and instruction for physiotherapy and evaluation in a radiosurgery center. This case was discussed in our Department's Monthly Interinstitutional Pediatric Neuroscience Meeting. Α possible surgical intervention, if needed in the future, was considered as another option in the armamentarium of the management strategy for this potentially life-threatening lesion. A multidisciplinary approach is particularly helpful in determining the optimal management plan of challenging cases in Pediatric Neurosurgery.

The locked-in syndrome (LiS) is defined as the loss of most voluntary muscle movements with preserved cognitive abilities due to a ventral pontine lesion. However, some patients may also have severe impairment of consciousness [locked-in plus syndrome (LiPS)]. Here we aimed to explore structural differences between LiS and LiPS patients of vascular aetiology, focusing on lesion patterns and locations to better delineate the clinical spectrum of LiS and LiPS. In this retrospective case series study, we report nine patients (two women), ages 29–74 years (median 50) with LiS and LiPS who were diagnosed between 2007 and 2021. Clinical parameters, MRI findings including the lesioned structures, and a shape feature calculation are presented for every patient. The lesioned structures were determined by a senior neuroradiologist. Two of nine patients had fully retained consciousness (LiS) and seven showed various degrees of impaired consciousness (LiPS). Lesions of LiS patients are round and confined to the pons, whereas lesions of LiPS patients are more elongated and reach neighbouring areas such as the mesencephalon, thalamus or ascending reticular activating system. Lesions involving the mesencephalon and the thalamus are strong indicators of LiPS, whereas for lesions restricted to the pons, the dorsal extension and the associated damage to the ascending reticular activating system are crucial to differentiate LiS from LiPS. Recognizing LiPS using clinical and radiological findings is important as these patients may need different therapies and care and, most importantly, should not be mistaken as unresponsive wakefulness syndrome. [ABSTRACT FROM AUTHOR]

Introduction: Diffuse midline glioma (DMG) of the pons occurs in pediatric patients and carries a dismal prognosis. Biopsy is not necessary for diagnosis but provides information, particularly H3K27M status, with prognostic implications. Additionally, biopsy information may open therapeutic options such as clinical trials that require mutation status. Therefore, we sought to assess the safety of surgical biopsy in DMG patients as well as its potential impact on clinical course. Methods: Retrospective analysis of patients who were radiographically and clinically diagnosed with pontine DMG in the last 5 years was performed. We assessed demographic, clinical, radiographic, surgical, and follow-up data. Results: 25 patients were included; 18 (72%) underwent biopsy while 7 (28%) declined. 12 biopsies (67%) were performed with robotic arm and 5 (27%) with frameless stereotaxy. Three biopsied patients (17%) experienced new post-operative neurologic deficits (1 facial palsy, 1 VI nerve palsy and 1 ataxia) that all resolved at 2-week follow-up. All biopsies yielded diagnostic tissue. Fourteen patients (78%) had H3K27M mutation. Median OS for H3K27M patients was 10 months compared to 11 months in the wild-type patients (p = 0.30, log-rank test). Median OS for patients enrolled in clinical trials was 12 months compared to 8 months for non-trial patients (p = 0.076). Conclusion: In our series, stereotactic pontine DMG biopsies did not carry any permanent deficit or complication and yielded diagnostic tissue in all patients. Similar post-operative course was observed in both robot-assisted and frameless stereotactic approaches. There was no significant difference in survival based on mutation status or clinical trial enrollment. [ABSTRACT FROM AUTHOR]

Most cases of sudden sensorineural hearing loss (SSNHL) occur without a specific identifiable cause, although vascular factors may serve as potential etiological contributors. Silent infarction refers to ischemic changes observed on imaging studies without accompanying clinical symptoms; however, this condition is clinically significant owing to the increased risk of future stroke. We report a case of left-sided SSNHL accompanied by dizziness in a 62-year-old male patient who was diagnosed with left pontine infarction without any other neurological symptoms. The cochlea and pons receive blood supply from the anterior inferior cerebellar artery; the cochlea lacks collateral vessels and is therefore susceptible to fluctuations in blood flow. This case report provides evidence to support the vascular hypothesis as the etiology underlying SSNHL. [ABSTRACT FROM AUTHOR]

We describe prenatal diagnosis of Poland-Möbius syndrome using a combination of ultrasound and MRI. Poland syndrome was diagnosed based on absence of the pectoralis muscles associated with dextroposition of the fetal heart and elevation of the left diaphragm. Associated brain anomalies that led to the diagnosis of Poland-Möbius syndrome, included ventriculomegaly, hypoplastic cerebellum, tectal beaking, and a peculiar flattening of the posterior aspect of the pons and medulla oblongata, which has been reported by postnatal diffusion tensor imaging studies as a reliable neuroimaging marker for Möbius syndrome. Since abnormalities of cranial nerves VI and VII may be difficult to detect prenatally, careful attention to the appearance of the brain stem as illustrated in the current report may aid in the prenatal diagnosis of Möbius syndrome. [ABSTRACT FROM AUTHOR]

In patients undergoing elective cardiovascular and thoracic surgery, malnutrition and the deterioration of nutritional status are associated with negative outcomes. Recognition of the contributory factors and the complications stemming from surgical stress is important for the prevention and management of these patients. We have reviewed the literature available and focused on the nutritional and metabolic aspects affecting surgical patients, with emphasis on the recommendations of enhanced recovery protocols. The implementation of enhanced recovery protocols and nutritional support guidelines focusing on the surgical patient as part of a multidisciplinary approach would improve the nutritional status of surgical patients at risk for negative outcomes [ABSTRACT FROM AUTHOR]

We review the latest developments in Fiber-optic Telecommunications and Networks presented at OFC 2023 and compare the progress accomplished in the previous years. Topics of interest this year and discussed in this review include Long Haul and Intra Data Centers communications, Optical switches, sensors in submarine communications, some invited presentations (alas without papers such as in Optical Computers!), Secure Communications through Quantum effects, and Passive Optical Networks, PONs [ABSTRACT FROM AUTHOR]

This series lists a pictorial quiz pertaining to identification of normal and abnormal anatomical structures and landmarks at a given level on computed tomography (CT). Readers are expected to identify and appreciate the changes from normal anatomy and variations of a given pathology. The main structures assessed in this quiz are the pons, ventricular system of the brain, and the basal cisterns. Particular emphasis is placed on the presentations of intra-cranial haemorrhages, particularly sub-arachnoid and epidural haemorrhages, and masses around the region of the pons, midbrain and cerebellum. There is also a question pertaining to increased intracranial pressure. Differential diagnoses are also given where necessary to guide clinical practice and further learning. A Points to remember section details key clinical pearls. Furthermore, key resources have been cited as recommendations for further reading. It is anticipated that this series will enhance the understanding of sectional anatomy of the brain to aid in brain CT interpretation.

Behcet's disease (BD) is a multisystem, autoimmune vasculitis disorder affecting small, medium, and large blood vessels, with poorly understood pathogenesis. It commonly presents with recurrent aphthous ulcers, genital ulcers, skin lesions, and bilateral uveitis. Neurological symptoms are present in less than 10% of cases and develop, on average, 5-6 years after the first non-neurological symptoms. This presentation, known as Neuro-Behcet's disease (NBD), is associated with a worse prognosis of BD. Treatment for NBD is dependent on the severity of symptoms and the presence of other systemic manifestations but often initially involves glucocorticoids and a disease-modifying agent. This case report presents a 44-year-old female patient, previously diagnosed with BD, who presented with neurological symptoms and MRI findings consistent with NBD.

Background Developmental venous anomaly (DVA) is a benign venous abnormality draining normal brain parenchyma. It is mostly asymptomatic; however, rare complications such as hemorrhage may lead to symptomatic conditions. Headache and seizure are the most common symptoms. Hearing loss is an extremely rare presentation of DVA. To our knowledge, only five cases of DVA, presenting with hearing loss, had been reported so far. Case Presentation We report the case of a 27-year-old woman who presented with a sensorineural hearing loss followed by facial paresis. Magnetic resonance imaging (MRI) and computed tomography (CT) angiography revealed hematoma with adjacent converging veins showing a typical "caput medusa" sign in the left middle cerebellar peduncle, in favor of DVA. Due to the compression effect of hematoma, she underwent surgery. Hearing loss and facial paresis improved significantly during the postoperative follow-up. Conclusion Although DVA is mostly benign and asymptomatic, complications such as hemorrhage rarely occur. Hearing loss is an extremely rare presentation that can be attributable to the compression effect on the cranial nerve VII to VIII complex. In the case of compression effect or progression of symptoms, surgical intervention is necessary. A good clinical outcome could be expected postoperatively. [ABSTRACT FROM AUTHOR]

Summary: Important brainstem regions are involved in the regulation of rapid eye movement sleep. We hypothesized that brainstem stroke is associated with dysregulated rapid eye movement sleep and related muscle activity. We compared quantitative/qualitative polysomnography features of rapid eye movement sleep and muscle activity (any, phasic, tonic) between 15 patients with brainstem stroke (N = 46 rapid eye movement periods), 16 patients with lacunar/non‐brainstem stroke (N = 40 rapid eye movement periods), 15 healthy controls (N = 62 rapid eye movement periods), and patients with Parkinson's disease and polysomnography‐confirmed rapid eye movement sleep behaviour disorder. Further, in the brainstem group, we performed a magnetic resonance imaging‐based lesion overlap analysis. The mean ratio of muscle activity to rapid eye movement sleep epoch in the brainstem group ("any" muscle activity 0.09 ± 0.15; phasic muscle activity 0.08 ± 0.14) was significantly lower than in the lacunar group ("any" muscle activity 0.17 ± 0.2, p < 0.05; phasic muscle activity 0.16 ± 0.19, p < 0.05), and also lower than in the control group ("any" muscle activity 0.15 ± 0.17, p < 0.05). Magnetic resonance imaging‐based lesion analysis indicated an area of maximum overlap in the medioventral pontine region for patients with reduced phasic muscle activity index. For all groups, mean values of muscle activity were significantly lower than in the patients with Parkinson's disease and polysomnography‐confirmed REM sleep behaviour disorder group ("any" activity 0.51 ± 0.26, p < 0.0001 for all groups; phasic muscle activity 0.42 ± 0.21, p < 0.0001 for all groups). For the tonic muscle activity in the mentalis muscle, no significant differences were found between the groups. In the brainstem group, contrary to the lacunar and the control groups, "any" muscle activity index during rapid eye movement sleep was significantly reduced after the third rapid eye movement sleep phase. This study reports on the impact of brainstem stroke on rapid eye movement atonia features in a human cohort. Our findings highlight the important role of the human brainstem, in particular the medioventral pontine regions, in the regulation of phasic muscle activity during rapid eye movement sleep and the ultradian distribution of rapid eye movement‐related muscle activity. [ABSTRACT FROM AUTHOR]

An 18-year-old man presented with the complaints of occasional headache and limb weakness associated with slurring of speech and purposeless laughing. Magnetic resonance imaging showed a diffuse altered signal intensity area involving the pons with asymmetrical expansion. The patient underwent surgical resection. Histology was suggestive of a WHO grade IV glioblastoma. Pathological laughing in a patient with a pontine lesion is a very rare presentation. Evidence for a mechanism of action underpinning how pontine lesions can cause such behavioral changes through the disruption of a network of cerebro-ponto-cerebellar pathways is discussed. [ABSTRACT FROM AUTHOR]

The locked-in syndrome (LiS) is characterized by quadriplegia with preserved vertical eye and eyelid movements and retained cognitive abilities. Subcategorization, aetiologies and the anatomical foundation of LiS are discussed. The damage of different structures in the pons, mesencephalon and thalamus are attributed to symptoms of classical, complete and incomplete LiS and the locked-in plus syndrome, which is characterized by additional impairments of consciousness, making the clinical distinction to other chronic disorders of consciousness at times difficult. Other differential diagnoses are cognitive motor dissociation (CMD) and akinetic mutism. Treatment options are reviewed and an early, interdisciplinary and aggressive approach, including the provision of psychological support and coping strategies is favoured. The establishment of communication is a main goal of rehabilitation. Finally, the quality of life of LiS patients and ethical implications are considered. While patients with LiS report a high quality of life and well-being, medical professionals and caregivers have largely pessimistic perceptions. The negative view on life with LiS must be overthought and the autonomy and dignity of LiS patients prioritized. Knowledge has to be disseminated, diagnostics accelerated and technical support system development promoted. More well-designed research but also more awareness of the needs of LiS patients and their perception as individual persons is needed to enable a life with LiS that is worth living. [ABSTRACT FROM AUTHOR]

A solitary pontine lesion (SPL) is a single brainstem lesion on the trigeminal nerve pathway without any other central nervous system lesion. This research aimed to investigate the demographic and clinical features of nonpainful TNO patients with SPL and identify the most frequently affected anatomical areas using lesion mapping techniques. Demographic and clinical features were retrospectively reviewed from the patients' charts. Brain lesions were mapped using MRIcroGL software. The study included 6 patients (three females and three males) with an SPL. The median age of the patients was 57 (range: 46–68) years. Cranial MRI displayed lesions in the dorsolateral pons and the cerebellar peduncle. The lesion mapping revealed that the lesions were on the trigeminal nerve pathway. SPL is an uncommon cause of TNO. Nonpainful SPL patients have demographic, clinical, and radiological features similar to those of painful SPL patients. The lesion mapping showed that the same brainstem areas are affected in painful and nonpainful SPL patients. [ABSTRACT FROM AUTHOR]

Measurement of brainstem diameters (midbrain, pons, and medulla oblongata)is of potential clinical significance, as changes in brainstem size may decrease or increase due to age, neurodegenerative disorders, or neoplasms. In human medicine, numerous studies have reported the normal reference range of brainstem size, which is hitherto unexplored in veterinary medicine, particularly for small-breed dogs. Therefore, this study aims to investigate the reference range of brainstem diameters in small-breed dogs and to correlate the measurements with age, body weight (BW), and body condition score (BCS). Herein, magnetic resonance (MR) images of 544 small-breed dogs were evaluated. Based on the exclusion criteria, 193 dogs were included in the midbrain and pons evaluation, and of these, 119 dogs were included in the medulla oblongata evaluation. Using MR images, the height and width of the midbrain, pons, and medulla oblongata were measured on the median and transverse plane on the T1-weighted image. For the medulla oblongata, two points were measured for each height and width. The mean values of midbrain height (MH), midbrain width (MW), pons height (PH), pons width (PW), medulla oblongata height at the fourth ventricle level (MOHV), medulla oblongata height at the cervicomedullary (CM) junction level (MOHC), rostral medulla oblongata width (RMOW), and caudal medulla oblongata width (CMOW) were 7.18 ± 0.56 mm, 17.42 ± 1.21 mm, 9.73 ± 0.64 mm, 17.23 ± 1.21 mm, 6.06 ± 0.53 mm, 5.77 ± 0.40 mm, 18.93 ± 1.25 mm, and 10.12 ± 1.08 mm, respectively. No significant differences were found between male and female dogs for all the measurements. A negative correlation was found between age and midbrain diameter, including MH (p < 0.001) and MW (p = 0.002). All brainstem diameters were correlated positively with BW (p < 0.05). No significant correlation was found between BCS and all brainstem diameters. Brainstem diameters differed significantly between breeds (p < 0.05), except for MW (p = 0.137). This study assessed linear measurements of the brainstem diameter in small-breed dogs. We suggest that these results could be useful in assessing abnormal conditions of the brainstem in small-breed dogs.

Background and aim: Cerebellar infarction (CI) is a serious cerebrovascular disease that may present with non-focal neurological deficits, leading to delay of clinical recognition and treatment. The aim of this study is to investigate the variability of symptoms, diagnostic outcomes and early prognosis in patients with cerebellar infarction compared with pontine infarction (PI). Methods: Between 2012 and 2014, a total of 79 patients (68 ± 14 years, female sex 42%, median NIHSS score: 5) with CI (43) and PI (36) were included and analyzed. Results: CI patients were admitted to emergency department one hour earlier compared with patients with PI. The most common symptoms in CI were dysarthria (67%), impaired coordination (61%), limb weakness (54%), dizziness/vertigo (49%), gait and stance uncertainty (42%), nausea or/and vomiting (42%), nystagmus (37%), dysphagia (30%) and headache (26%). Nineteen patients (44%) had symptomatic stenosis and two patients had vertebral artery dissection on duplex sonography and MR angiography.Four patients (9%) received a systemic intravenous thrombolysis with rt-PA and three patients received mechanical thrombectomy.Three months after the event, five patients (12%) had died and 15 (40) had disability with mRS (3–5). Conclusions: Cerebellar infarction occurs with a high variability of symptoms and should be considered when non-focal symptoms are present.

The term "Osmotic Demyelination Syndrome" (ODS) is synonymous with central pontine myelinolysis (CPM), denoting a condition characterised by brain damage, particularly affecting the white matter tracts of the pontine region. This damage arises due to the rapid correction of metabolic imbalances, primarily cases of hyponatremia. Noteworthy triggers encompass severe burns, liver transplantations, anorexia nervosa, hyperemesis gravidarum, and hyperglycaemia, all linked to the development of CPM. Clinical manifestations encompass a spectrum of signs and symptoms, including dysphagia, dysarthria, spastic quadriparesis, pseudobulbar paralysis, ataxia, lethargy, tremors, disorientation, catatonia, and, in severe instances, locked-in syndrome and coma. A recent case involving a 45-year-old woman illustrates these complexities. Upon admission to the Medicine Intensive Care Unit, she presented with symptoms indicative of diminished responsiveness and bilateral weakness in the upper and lower limbs. Of significance, the patient had a pre-existing medical history of hyperthyroidism. Extensive diagnostic investigations were undertaken, revealing compelling evidence of profound hyponatremia through blood analyses. Furthermore, magnetic resonance imaging (MRI) was performed, unveiling conspicuous areas of abnormal hyperintensity located in the central pons, intriguingly accompanied by spared peripheral regions. These radiological findings align with the characteristic pattern associated with osmotic demyelination syndrome, illuminating the underlying pathology. [ABSTRACT FROM AUTHOR]

This series lists a pictorial quiz pertaining to identification of normal and abnormal anatomical structures and landmarks at a given level on computed tomography (CT). Readers are expected to identify and appreciate the changes from normal anatomy and variations of a given pathology. The main structures assessed in this quiz are the pons, ventricular system of the brain, and the basal cisterns. Particular emphasis is placed on the presentations of intra-cranial haemorrhages, particularly sub-arachnoid and epidural haemorrhages, and masses around the region of the pons, midbrain and cerebellum. There is also a question pertaining to increased intracranial pressure. Differential diagnoses are also given where necessary to guide clinical practice and further learning. A Points to remember section details key clinical pearls. Furthermore, key resources have been cited as recommendations for further reading. It is anticipated that this series will enhance the understanding of sectional anatomy of the brain to aid in brain CT interpretation. [ABSTRACT FROM AUTHOR]