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Neuroscience Bulletin Feb 2009Perivascular space (PVS) is a crevice between two slices of cerebral pia maters, filled with tissue fluid, which be formed by pia mater emboling in the surrounding of... (Review)
Review
Perivascular space (PVS) is a crevice between two slices of cerebral pia maters, filled with tissue fluid, which be formed by pia mater emboling in the surrounding of cerebral perforating branch (excluding micrangium). Normal PVS (diameter < 2 mm) can be found in almost all healthy adults; however enlarged PVS (diameter > 2 mm) has correlation with neurological disorders probably. The article reviews the formation mechanism, imageology characteristics and the relation with neurological disorders of PVS, which is beneficial to the research of some neurological disorders etiopathogenesis and treatment.
Topics: Animals; Blood Vessels; Humans; Nervous System Diseases; Pia Mater
PubMed: 19190687
DOI: 10.1007/s12264-009-1103-0 -
Journal of Anatomy Jun 1990Biopsies of histologically normal adult human cerebral cortex, underlying white matter and overlying leptomeninges were taken from frontal and temporal lobectomy...
Biopsies of histologically normal adult human cerebral cortex, underlying white matter and overlying leptomeninges were taken from frontal and temporal lobectomy specimens excised during the removal of cerebral tumours. Multiple blocks from 6 patients (aged 18-53 years) were examined by light and transmission electron microscopy. A thin sheath of pia mater cells was found to surround completely arterioles and arteries in the brain, in the subpial space and in the subarachnoid space. Pia mater cells, forming the perivascular sheath, were identified by the presence of desmosomes or small nexus junctions and by continuity with the pia mater itself. The presence of the pial sheath suggests that the perivascular spaces around intracerebral arteries are in direct continuity with the perivascular spaces around subarachnoid arteries. No similar pial sheath was observed around intracerebral or subpial venules. The role of the periarterial spaces, enclosed by the pial sheath, is discussed in relation to the results of physiological experiments suggesting drainage of interstitial fluid from brain tissue into the perivascular pathways along major cerebral arteries in the subarachnoid space. As arterioles in the brain become smaller and lose their smooth muscle coats, the pial sheath becomes incomplete. The anatomical relationships between the pia mater and blood vessels in the human cerebrum is summarised diagrammatically, and a possible role for pial cells as an enzymic barrier protecting the brain from exogenous catecholamines is discussed.
Topics: Adolescent; Adult; Arterioles; Brain; Cerebral Cortex; Female; Humans; Male; Microscopy, Electron; Middle Aged; Pia Mater; Regional Blood Flow; Subarachnoid Space; Venules
PubMed: 2254158
DOI: No ID Found -
Nature Communications Jul 2022Perivascular spaces (PVS) drain brain waste metabolites, but their specific flow paths are debated. Meningeal pia mater reportedly forms the outermost boundary that...
Perivascular spaces (PVS) drain brain waste metabolites, but their specific flow paths are debated. Meningeal pia mater reportedly forms the outermost boundary that confines flow around blood vessels. Yet, we show that pia is perforated and permissive to PVS fluid flow. Furthermore, we demonstrate that pia is comprised of vascular and cerebral layers that coalesce in variable patterns along leptomeningeal arteries, often merging around penetrating arterioles. Heterogeneous pial architectures form variable sieve-like structures that differentially influence cerebrospinal fluid (CSF) transport along PVS. The degree of pial coverage correlates with macrophage density and phagocytosis of CSF tracer. In vivo imaging confirms transpial influx of CSF tracer, suggesting a role of pia in CSF filtration, but not flow restriction. Additionally, pial layers atrophy with age. Old mice also exhibit areas of pial denudation that are not observed in young animals, but pia is unexpectedly hypertrophied in a mouse model of Alzheimer's disease. Moreover, pial thickness correlates with improved CSF flow and reduced β-amyloid deposits in PVS of old mice. We show that PVS morphology in mice is variable and that the structure and function of pia suggests a previously unrecognized role in regulating CSF transport and amyloid clearance in aging and disease.
Topics: Aging; Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Glymphatic System; Mice
PubMed: 35794106
DOI: 10.1038/s41467-022-31257-9 -
BioRxiv : the Preprint Server For... Aug 2023The recent characterization of the glymphatic system and meningeal lymphatics has re-emphasized the role of the meninges in facilitating CSF transport and clearance....
BACKGROUND
The recent characterization of the glymphatic system and meningeal lymphatics has re-emphasized the role of the meninges in facilitating CSF transport and clearance. Here, we characterize small and large CSF solute distribution patterns along the intracranial and surface meninges in neonatal rodents and compare our findings to a rodent model of intraventricular hemorrhage-posthemorrhagic hydrocephalus. We also examine CSF interactions with the tela choroidea and its pial invaginations into the choroid plexuses of the lateral, third, and fourth ventricles.
METHODS
1.9-nm gold nanoparticles, 15-nm gold nanoparticles, or 3 kDa Red Dextran Tetramethylrhodamine constituted in aCSF were infused into the right lateral ventricle of P7 rats to track CSF circulation. 10 minutes post-1.9-nm gold nanoparticle and Red Dextran Tetramethylrhodamine injection and 4 hours post-15-nm gold nanoparticle injection, animals were sacrificed and brains harvested for histologic analysis to identify CSF tracer localization in the cranial and spine meninges and choroid plexus. Spinal dura and leptomeninges (arachnoid and pia) wholemounts were also performed.
RESULTS
There was significantly less CSF tracer distribution in the dura compared to the arachnoid and pia maters in neonatal rodents. Both small and large CSF tracers were transported intracranially to the arachnoid and pia mater of the perimesencephalic cisterns and tela choroidea, but not the dura mater of the falx cerebri. CSF tracers followed a similar distribution pattern in the spinal meninges. In the choroid plexus, there was large CSF tracer distribution in the apical surface of epithelial cells, and small CSF tracer along the basolateral surface. There were no significant differences in tracer intensity in the intracranial meninges of control vs. intraventricular hemorrhage-posthemorrhagic hydrocephalus (PHH) rodents, indicating preserved meningeal transport in the setting of PHH.
CONCLUSIONS
Differential CSF tracer handling by the leptomeninges suggests that there are distinct roles for CSF handling between the arachnoid-pia and dura maters in the developing brain. Similarly, differences in apical vs. luminal choroid plexus CSF handling may provide insight into particle-size dependent CSF transport at the CSF-choroid plexus border.
PubMed: 37645776
DOI: 10.1101/2023.08.10.552826 -
Interventional Neuroradiology : Journal... Dec 2015The arterial blood supply to the dura mater is rich, complex and is derived from both the internal and external carotid systems. Endovascular management of a variety of...
The arterial blood supply to the dura mater is rich, complex and is derived from both the internal and external carotid systems. Endovascular management of a variety of intracranial diseases necessitates a thorough understanding of the dural arterial network. In this article we review the normal contributions of the pial arteries to the blood supply of the dura mater and discuss some aspects of its role in the supply of dural arteriovenous shunts (DAVS).
Topics: Anatomic Landmarks; Dura Mater; Humans; Pia Mater; Reference Values
PubMed: 26494407
DOI: 10.1177/1591019915609137 -
Acta Ophthalmologica Jun 2014To assess the histologic correlate of the peripapillary ring (PPR) as the optic disc boundary, to measure it histomorphometrically and to assess its associations with...
PURPOSE
To assess the histologic correlate of the peripapillary ring (PPR) as the optic disc boundary, to measure it histomorphometrically and to assess its associations with glaucoma and axial length.
METHODS
Using a light microscope, we measured the width of the PPR and optic nerve pia mater. We additionally had measured the axial length, length of parapapillary beta and gamma zones, and thickness of the sclera and choroid.
RESULTS
The study included 83 human globes with a mean axial length of 26.1 ± 3.3 mm (range: 20.0-35.0 mm). In the non-highly myopic (axial length <26.5 mm) non-glaucomatous eyes, mean PPR width was 55 ± 14 μm (range: 26-88 μm) and mean thickness of the optic nerve pia mater was 52 ± 22 μm (range: 20-84 μm). PPR width and pia mater thickness were significantly associated with each other (p = 0.001; correlation coefficient r = 0.37). PPR width increased significantly with longer axial length (p = 0.001; r = 0.35) and with the length of the peripapillary scleral flange (p = 0.02; r = 0.34). Pia mater thickness increased significantly with longer axial length (p = 0.03; r = 0.24) and with presence of glaucoma (p = 0.03). In eyes without parapapillary gamma zone, PPR was covered or was at least touched by the end of Bruch's membrane and separated the peripapillary choroid from the prelaminar optic nerve head tissue. In eyes with parapapillary gamma zone, PPR was the continuation of the optic nerve pia mater and reached the undersurface of the peripapillary retinal nerve fibre layer. In these eyes, Bruch's membrane started in a distance of up to 5 mm from PPR, and the thin space of peripapillary choroid ended by an attachment of Bruch's membrane to the thinned sclera.
CONCLUSIONS
Peripapillary ring width (mean: 55 ± 14 μm) increases slightly with longer axial length and is independent of glaucoma. It is strongly correlated with the pia mater thickness and is the continuation of the pia mater to the ocular surface.
Topics: Adult; Aged; Aged, 80 and over; Axial Length, Eye; Eye Enucleation; Female; Glaucoma; Humans; Intraocular Pressure; Male; Middle Aged; Myopia, Degenerative; Optic Disk; Young Adult
PubMed: 24373493
DOI: 10.1111/aos.12324 -
Investigative Ophthalmology & Visual... Aug 2020To test whether mice with microfibril deficiency due to the Tsk mutation of fibrillin-1 (Fbn1Tsk/+) have increased susceptibility to pressure-induced retinal ganglion...
PURPOSE
To test whether mice with microfibril deficiency due to the Tsk mutation of fibrillin-1 (Fbn1Tsk/+) have increased susceptibility to pressure-induced retinal ganglion cell (RGC) degeneration.
METHODS
Intraocular pressure (IOP) elevation was induced in Fbn1Tsk/+ and wild type (wt) mice by injecting microbeads into the anterior chamber. Mice were then followed up for four months, with IOP measurements every three to six days. Retinas were stained for Brn3a to determine RGC number. Optic nerve cross-sections were stained with p-phenylene diamine to determine nerve area, axon number, and caliber and thickness of the pia mater.
RESULTS
Microbead injection induced significant IOP elevation that was significantly less for Fbn1Tsk/+ mice compared with wt. The optic nerves and optic nerve axons were larger, and the elastic fiber-rich pia mater was thinner in Fbn1Tsk/+ mice. Microbead injection resulted in reduced optic nerve size, thicker pia mater, and a slight decrease in axon size. Fbn1Tsk/+ mice had significantly greater loss of RGCs and optic nerve axons compared with wt (14.8% vs. 5.8%, P = 0.002, and 17.0% vs. 7.5%, P = 0.002, respectively).
CONCLUSIONS
Fbn1Tsk/+mice had altered optic nerve structure as indicated by larger optic nerves, larger optic nerve axons and thinner pia mater, consistent with our previous findings. Despite lower IOP elevation, Fbn1Tsk/+mice had greater loss of RGCs and optic nerve axons, suggesting increased susceptibility to IOP-induced optic nerve degeneration in microfibril-deficient mice.
Topics: Animals; Disease Susceptibility; Female; Fibrillin-1; Glaucoma; Intraocular Pressure; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microfibrils; Optic Nerve; Retina; Retinal Ganglion Cells
PubMed: 32797197
DOI: 10.1167/iovs.61.10.28 -
Nature Medicine Jan 2020Gene silencing with virally delivered shRNA represents a promising approach for treatment of inherited neurodegenerative disorders. In the present study we develop a...
Gene silencing with virally delivered shRNA represents a promising approach for treatment of inherited neurodegenerative disorders. In the present study we develop a subpial technique, which we show in adult animals successfully delivers adeno-associated virus (AAV) throughout the cervical, thoracic and lumbar spinal cord, as well as brain motor centers. One-time injection at cervical and lumbar levels just before disease onset in mice expressing a familial amyotrophic lateral sclerosis (ALS)-causing mutant SOD1 produces long-term suppression of motoneuron disease, including near-complete preservation of spinal α-motoneurons and muscle innervation. Treatment after disease onset potently blocks progression of disease and further α-motoneuron degeneration. A single subpial AAV9 injection in adult pigs or non-human primates using a newly designed device produces homogeneous delivery throughout the cervical spinal cord white and gray matter and brain motor centers. Thus, spinal subpial delivery in adult animals is highly effective for AAV-mediated gene delivery throughout the spinal cord and supraspinal motor centers.
Topics: Amyotrophic Lateral Sclerosis; Animals; Atrophy; Dependovirus; Disease Progression; Evoked Potentials, Motor; Female; Gene Expression Regulation; Gene Silencing; Gene Transfer Techniques; Humans; Inflammation; Interneurons; Male; Mice, Inbred C57BL; Mice, Transgenic; Motor Neurons; Muscle Development; Nerve Degeneration; Pia Mater; Primates; Protein Folding; RNA, Messenger; RNA, Small Interfering; Spinal Cord; Superoxide Dismutase-1; Swine
PubMed: 31873312
DOI: 10.1038/s41591-019-0674-1 -
Neurobiology of Disease Oct 2020Blood dynamically and richly supplies the cerebral tissue via microvessels invested in pia matter perforating the cerebral substance. Arteries penetrating the cerebral... (Review)
Review
Structure and function of the perivascular fluid compartment and vertebral venous plexus: Illumining a novel theory on mechanisms underlying the pathogenesis of Alzheimer's, cerebral small vessel, and neurodegenerative diseases.
Blood dynamically and richly supplies the cerebral tissue via microvessels invested in pia matter perforating the cerebral substance. Arteries penetrating the cerebral substance derive an investment from one or two successive layers of pia mater, luminally apposed to the pial-glial basal lamina of the microvasculature and abluminally apposed to a series of aquaporin IV-studded astrocytic end feet constituting the soi-disant glia limitans. The full investment of successive layers forms the variably continuous walls of the periarteriolar, pericapillary, and perivenular divisions of the perivascular fluid compartment. The pia matter disappears at the distal periarteriolar division of the perivascular fluid compartment. Plasma from arteriolar blood sequentially transudates into the periarteriolar division of the perivascular fluid compartment and subarachnoid cisterns in precession to trickling into the neural interstitium. Fluid from the neural interstitium successively propagates into the venules through the subarachnoid cisterns and perivenular division of the perivascular fluid compartment. Fluid fluent within the perivascular fluid compartment flows gegen the net direction of arteriovenular flow. Microvessel oscillations at the central tendency of the cerebral vasomotion generate corresponding oscillations of within the surrounding perivascular fluid compartment, interposed betwixt the abluminal surface of the vessels and internal surface of the pia mater. The precise microanatomy of this most fascinating among designable spaces has eluded the efforts of various investigators to interrogate its structure, though most authors non-consensusly concur the investing layers effectively and functionally segregate the perivascular and subarachnoid fluid compartments. Enlargement of the perivascular fluid compartment in a variety of neurological disorders, including senile dementia of the Alzheimer's type and cerebral small vessel disease, may alternately or coordinately constitute a correlative marker of disease severity and a possible cause implicated in the mechanistic pathogenesis of these conditions. Venular pressures modulating oscillatory dynamic flow within the perivascular fluid compartment may similarly contribute to the development of a variety among neurological disorders. An intimate understanding of subtle features typifying microanatomy and microphysiology of the investing structures and spaces of the cerebral microvasculature may powerfully inform mechanistic pathophysiology mediating a variety of neurovascular ischemic, neuroinfectious, neuroautoimmune, and neurodegenerative diseases.
Topics: Alzheimer Disease; Cerebral Small Vessel Diseases; Glymphatic System; Humans; Microvessels; Neurodegenerative Diseases; Venous Pressure
PubMed: 32687942
DOI: 10.1016/j.nbd.2020.105022 -
Interventional Neuroradiology : Journal... Oct 2016An intracranial non-galenic pial arteriovenous fistula (NGPAVF) is a direct connection between the intracranial artery and vein without a nidus. NGPAVFs are clinically... (Review)
Review
An intracranial non-galenic pial arteriovenous fistula (NGPAVF) is a direct connection between the intracranial artery and vein without a nidus. NGPAVFs are clinically rare, and the current understanding of NGPAVFs is limited. This study searched PubMed for the currently available literature, and a review of the relevant publications revealed that NGPAVFs require aggressive treatment, spontaneous occlusion is uncommon, and the prognosis following conservative treatment is poor. NGPAVFs can be divided into congenital and traumatic (including iatrogenic) types. Clinically, NGPAVFs are characterized by congestive heart failure, epilepsy, hemorrhage, mass effects, and nerve function deficits. For the imaging examination of NGPAVFs, digital subtraction angiography (DSA) is still the gold standard for diagnosis, although magnetic resonance DSA (MRDSA) and 4D computed tomography angiography (CTA) can also provide hemodynamic data in a non-invasive manner. Current treatments for NGPAVFs include surgical resection and endovascular embolization, both of which can yield clinical improvements. However, potential postoperative complications should be addressed, such as fatal bleeding due to rupture and deep vein thrombosis. Some studies recommend postoperative anticoagulation to reduce postoperative thrombotic complications.
Topics: Diagnosis, Differential; Diagnostic Imaging; Humans; Intracranial Arteriovenous Malformations; Pia Mater; Risk Factors
PubMed: 27388601
DOI: 10.1177/1591019916653934