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Microbiology Spectrum Mar 2017Central nervous system tuberculosis (CNS-TB) takes three clinical forms: meningitis (TBM), intracranial tuberculoma, and spinal arachnoiditis. TBM predominates in the... (Review)
Review
Central nervous system tuberculosis (CNS-TB) takes three clinical forms: meningitis (TBM), intracranial tuberculoma, and spinal arachnoiditis. TBM predominates in the western world and presents as a subacute to chronic meningitis syndrome with a prodrome of malaise, fever, and headache progressing to altered mentation and focal neurologic signs, followed by stupor, coma, and death within five to eight weeks of onset. The CSF formula typically shows a lymphocytic pleocytosis, and low glucose and high protein concentrations. Diagnosis rests on serial samples of CSF for smear and culture, combined with CSF PCR. Brain CT and MRI aid in diagnosis, assessment for complications, and monitoring of the clinical course. In a patient with compatible clinical features, the combination of meningeal enhancement and any degree of hydrocephalus is strongly suggestive of TBM. Vasculitis leading to infarcts in the basal ganglia occurs commonly and is a major determinant of morbidity and mortality. Treatment is most effective when started in the early stages of disease, and should be initiated promptly on the basis of strong clinical suspicion without waiting for laboratory confirmation. The initial 4 drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol) covers the possibility of infection with a resistant strain, maximizes antimicrobial impact, and reduces the likelihood of emerging resistance on therapy. Adjunctive corticosteroid therapy has been shown to reduce morbidity and mortality in all but late stage disease.
Topics: Anti-Inflammatory Agents; Antitubercular Agents; Arachnoiditis; Brain; Cerebrospinal Fluid; Humans; Magnetic Resonance Imaging; Mycobacterium; Polymerase Chain Reaction; Tomography, X-Ray Computed; Tuberculoma, Intracranial; Tuberculosis, Meningeal
PubMed: 28281443
DOI: 10.1128/microbiolspec.TNMI7-0044-2017 -
Genesis (New York, N.Y. : 2000) May 2019The meninges are membranous layers surrounding the central nervous system. In the head, the meninges lie between the brain and the skull, and interact closely with both... (Review)
Review
The meninges are membranous layers surrounding the central nervous system. In the head, the meninges lie between the brain and the skull, and interact closely with both during development. The cranial meninges originate from a mesenchymal sheath on the surface of the developing brain, called primary meninx, and undergo differentiation into three layers with distinct histological characteristics: the dura mater, the arachnoid mater, and the pia mater. While genetic regulation of meningeal development is still poorly understood, mouse mutants and other models with meningeal defects have demonstrated the importance of the meninges to normal development of the calvaria and the brain. For the calvaria, the interactions with the meninges are necessary for the progression of calvarial osteogenesis during early development. In later stages, the meninges control the patterning of the skull and the fate of the sutures. For the brain, the meninges regulate diverse processes including cell survival, cell migration, generation of neurons from progenitors, and vascularization. Also, the meninges serve as a stem cell niche for the brain in the postnatal life. Given these important roles of the meninges, further investigation into the molecular mechanisms underlying meningeal development can provide novel insights into the coordinated development of the head.
Topics: Animals; Arachnoid; Brain; Cell Differentiation; Developmental Biology; Dura Mater; Humans; Meninges; Pia Mater; Skull
PubMed: 30801905
DOI: 10.1002/dvg.23288 -
Neuron Dec 2023Leptomeninges, consisting of the pia mater and arachnoid, form a connective tissue investment and barrier enclosure of the brain. The exact nature of leptomeningeal...
Leptomeninges, consisting of the pia mater and arachnoid, form a connective tissue investment and barrier enclosure of the brain. The exact nature of leptomeningeal cells has long been debated. In this study, we identify five molecularly distinct fibroblast-like transcriptomes in cerebral leptomeninges; link them to anatomically distinct cell types of the pia, inner arachnoid, outer arachnoid barrier, and dural border layer; and contrast them to a sixth fibroblast-like transcriptome present in the choroid plexus and median eminence. Newly identified transcriptional markers enabled molecular characterization of cell types responsible for adherence of arachnoid layers to one another and for the arachnoid barrier. These markers also proved useful in identifying the molecular features of leptomeningeal development, injury, and repair that were preserved or changed after traumatic brain injury. Together, the findings highlight the value of identifying fibroblast transcriptional subsets and their cellular locations toward advancing the understanding of leptomeningeal physiology and pathology.
Topics: Mice; Animals; Meninges; Arachnoid; Pia Mater; Choroid Plexus; Brain
PubMed: 37776854
DOI: 10.1016/j.neuron.2023.09.002 -
The Journal of Experimental Medicine Feb 2023Arachnoid granulations (AG) are poorly investigated. Historical reports suggest that they regulate brain volume by passively transporting cerebrospinal fluid (CSF) into...
Arachnoid granulations (AG) are poorly investigated. Historical reports suggest that they regulate brain volume by passively transporting cerebrospinal fluid (CSF) into dural venous sinuses. Here, we studied the microstructure of cerebral AG in humans with the aim of understanding their roles in physiology. We discovered marked variations in AG size, lobation, location, content, and degree of surface encapsulation. High-resolution microscopy shows that AG consist of outer capsule and inner stromal core regions. The fine and porous framework suggests uncharacterized functions of AG in mechanical CSF filtration. Moreover, internal cytokine and immune cell enrichment imply unexplored neuroimmune properties of these structures that localize to the brain-meningeal lymphatic interface. Dramatic age-associated changes in AG structure are additionally identified. This study depicts for the first time microscopic networks of internal channels that communicate with perisinus spaces, suggesting that AG subserve important functions as transarachnoidal flow passageways. These data raise new theories regarding glymphatic-lymphatic coupling and mechanisms of CSF antigen clearance, homeostasis, and diseases.
Topics: Humans; Bone Marrow; Arachnoid; Dura Mater; Lymphatic System; Lymphatic Vessels
PubMed: 36469302
DOI: 10.1084/jem.20220618 -
Cellular and Molecular Life Sciences :... Mar 2021Cerebrospinal fluid (CSF) is produced by the choroid plexuses within the ventricles of the brain and circulates through the subarachnoid space of the skull and spinal... (Review)
Review
Cerebrospinal fluid (CSF) is produced by the choroid plexuses within the ventricles of the brain and circulates through the subarachnoid space of the skull and spinal column to provide buoyancy to and maintain fluid homeostasis of the brain and spinal cord. The question of how CSF drains from the subarachnoid space has long puzzled scientists and clinicians. For many decades, it was believed that arachnoid villi or granulations, outcroppings of arachnoid tissue that project into the dural venous sinuses, served as the major outflow route. However, this concept has been increasingly challenged in recent years, as physiological and imaging evidence from several species has accumulated showing that tracers injected into the CSF can instead be found within lymphatic vessels draining from the cranium and spine. With the recent high-profile rediscovery of meningeal lymphatic vessels located in the dura mater, another debate has emerged regarding the exact anatomical pathway(s) for CSF to reach the lymphatic system, with one side favoring direct efflux to the dural lymphatic vessels within the skull and spinal column and another side advocating for pathways along exiting cranial and spinal nerves. In this review, a summary of the historical and contemporary evidence for the different outflow pathways will be presented, allowing the reader to gain further perspective on the recent advances in the field. An improved understanding of this fundamental physiological process may lead to novel therapeutic approaches for a wide range of neurological conditions, including hydrocephalus, neurodegeneration and multiple sclerosis.
Topics: Animals; Arachnoid; Cerebrospinal Fluid; Cranial Nerves; Ethmoid Bone; Humans; Lymph Nodes; Lymphatic Vessels; Spine
PubMed: 33427948
DOI: 10.1007/s00018-020-03706-5 -
Child's Nervous System : ChNS :... Nov 2021Multiple names within the literature refer to a clinical picture affecting infants and consisting of a large or fast growing head circumference with enlarged cortical... (Review)
Review
PURPOSE
Multiple names within the literature refer to a clinical picture affecting infants and consisting of a large or fast growing head circumference with enlarged cortical subarachnoid spaces (CSAS) while cranial sutures are open. This myriad of terms demonstrates the confusion about the entity, that may even group together different etiological processes. In this review, we aim to shed light on this matter in an effort to restate the defining features of the clinical picture and sum the evidence and current understanding of its pathophysiology and related imaging findings.
METHODS
Extensive and updated review of the literature with special focus on defining features, clinical history with long term evaluation and pathophysiological process.
RESULTS
Functional and molecular CSF studies as well as clinical evidence challenges the common pathophysiological theory based on non-functional arachnoid villi. Conversely, there is increasing evidence supporting cerebro-venous system abnormalities as the main pathophysiological factor. Additionally, long term cohorts studies show that it may have subtle but irreversible neurodevelopmental consequences.
CONCLUSION
Subarachnomegaly is an age-related condition of the infancy with radiological enlargement of CSAS and often self limiting course. However, considering the evidence on pathophysiology as outlined herein and long term outcome reports, further research effort is needed to assess the consequences of venous outflow impairment and enlarged CSAS and how this relates to imaging findings and neurodevelopment test results later in life.
Topics: Humans; Hyperemia; Infant; Subarachnoid Space
PubMed: 34687332
DOI: 10.1007/s00381-021-05328-z -
Arquivos de Neuro-psiquiatria Jun 2023
Topics: Humans; Arachnoiditis; Hydrocephalus
PubMed: 37379872
DOI: 10.1055/s-0043-1768159 -
Current Opinion in Infectious Diseases Oct 2020Subarachnoid neurocysticercosis (SUBNCC) is caused by a morphologically unique proliferative form of Taenia solium involving the subarachnoid spaces. Prolonged therapy... (Review)
Review
PURPOSE OF REVIEW
Subarachnoid neurocysticercosis (SUBNCC) is caused by a morphologically unique proliferative form of Taenia solium involving the subarachnoid spaces. Prolonged therapy based upon the pathophysiology of SUBNCC and long-term follow-up have shed light on the course of disease and led to highly improved outcomes.
RECENT FINDINGS
SUBNCC has a prolonged incubation period of between 10 and 25 years characterized by cyst proliferation and growth and invasion of contiguous spaces leading to mass effect (Stage 1). With induction of the host-immune responses, cysts degenerate leading to a predominately inflammatory arachnoiditis (Stage 2) causing hydrocephalus, infarcts, and other inflammatory based neurological manifestations. Inactive disease (Stage 3) may occur naturally but mostly is a result of successful treatment, which generally requires prolonged intensive anthelminthic and antiinflammatory treatments. Cerebral spinal fluid cestode antigen or cestode DNA falling to nondetectable levels predicts effective treatment. Prolonged treatment with extended follow-up has resulted in moderate disability and no mortality. Repeated short intensive 8-14-day courses of treatment are also used, but long-term outcomes and safety using this strategy are not reported.
SUMMARY
SUBNCC gives rise to a chronic arachnoiditis. Its unique ability to proliferate and induce inflammatory responses requires long-term anthelmintic and antiinflammatory medications.
Topics: Animals; Anthelmintics; Anti-Inflammatory Agents; Antigens, Helminth; Arachnoiditis; Humans; Magnetic Resonance Imaging; Neurocysticercosis; Subarachnoid Space; Taenia solium
PubMed: 32868512
DOI: 10.1097/QCO.0000000000000669 -
PloS One 2020The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates that post-SCI inflammation is severe...
The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates that post-SCI inflammation is severe but the role of reactive astrogliosis not well understood given its implication in ongoing inflammation as damaging or neuroprotective. We have completed an extensive systematic study with MRI, histopathology, proteomics and ELISA analyses designed to further define the severe protracted and damaging inflammation after SCI in a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68+/CD163- macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163- macrophage numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. Acutely increased levels of TNF-alpha, IL-1beta, IFN-gamma and other pro-inflammatory cytokines, chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have demonstrated a close association between progressive astrogliosis and reduction in the severity of inflammation.
Topics: Animals; Anti-Inflammatory Agents; Arachnoiditis; Astrocytes; Cytokines; Disease Models, Animal; Gliosis; Humans; Macrophages; Magnetic Resonance Imaging; Male; Myelin Sheath; Rats; Severity of Illness Index; Spinal Cord; Spinal Cord Injuries; Time Factors
PubMed: 32191733
DOI: 10.1371/journal.pone.0226584 -
Anaesthesia Jun 2013
Topics: Anesthesia, Obstetrical; Anesthesia, Spinal; Arachnoiditis; Female; Humans; Paraplegia; Pregnancy
PubMed: 23662755
DOI: 10.1111/anae.12248