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Concept: Dura mater

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The arachnoid mater is a delicate and avascular layer that lies in direct contact with the dura and is separated from the pia mater by the cerebrospinal fluid-filled subarachnoid space. The subarachnoid space is divided into cisterns named according to surrounding brain structures.

Concepts: Leptomeningeal collateral circulation, Spinal cord, Brain, Pia mater, Dura mater, Arachnoid mater, Cerebrospinal fluid, Meninges

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Object This study aims to show the relationship between clinical outcome in patients who underwent surgical decompression for Chiari malformation (CM) and postoperative imaging studies, with particular emphasis on the subarachnoid cisterns of the posterior fossa. Methods One hundred seventy-seven patients with CM, including 97 with syringomyelia, underwent posterior fossa decompressive surgery. Both the dura and arachnoid were opened in 150 of these patients, and 135 underwent reduction of the cerebellar tonsils. The patients' clinical signs and symptoms were evaluated at 2 time points after surgery. Their imaging studies were analyzed specifically for the size of the retrotonsillar and subtonsillar cisterns and the syringomyelic cavities. The authors evaluated the relationship between these imaging findings and clinical parameters. Results Clinical improvement correlated strongly with enlargement of the subarachnoid cisterns, and enlargement of the cisterns also correlated with reduction in size of the syrinx cavities. Symptoms related to syringomyelia responded to reduction in size of the syrinx cavities. Conclusions Surgical decompression of the posterior fossa should aim to create relatively large subarachnoid cisterns and reduce the size of the syrinx cavity. Reduction of the cerebellar tonsils by surgical means, together with duraplasty, achieves this goal and thereby improves the clinical outcome for patients with CM. An incidental observation of the study is that obesity increases the likelihood of headache in patients with CM.

Concepts: Medical diagnosis, Medical sign, Dura mater, Medicine, Meninges, Symptom, Syringomyelia, Arnold-Chiari malformation

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Dura mater healing is crucial to prevent cerebrospinal fluid (CSF) leaks after neurosurgical procedures. Biological mechanisms leading to dural closure are only partially understood and have been studied in animals exclusively. We studied an in vitro model of dural closure which uses human cells.

Concepts: Meninges, Cerebrospinal fluid, Dura mater

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The mechanical mismatch between soft neural tissues and stiff neural implants hinders the long-term performance of implantable neuroprostheses. Here, we designed and fabricated soft neural implants with the shape and elasticity of dura mater, the protective membrane of the brain and spinal cord. The electronic dura mater, which we call e-dura, embeds interconnects, electrodes, and chemotrodes that sustain millions of mechanical stretch cycles, electrical stimulation pulses, and chemical injections. These integrated modalities enable multiple neuroprosthetic applications. The soft implants extracted cortical states in freely behaving animals for brain-machine interface and delivered electrochemical spinal neuromodulation that restored locomotion after paralyzing spinal cord injury.

Concepts: Arachnoid mater, Dura mater, Meninges, Spinal cord, Neuroprosthetics, Central nervous system, Brain

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In traumatic brain injury (TBI), membranes such as the dura mater, arachnoid mater, and pia mater play a vital role in transmitting motion from the skull to brain tissue. Magnetic Resonance Elastography (MRE) is an imaging technique developed for non-invasive estimation of soft tissue material parameters. In MRE, dynamic deformation of brain tissue is induced by skull vibrations; however skull motion and its mode of transmission to the brain remain largely uncharacterized. In this study, displacements of points in the skull, reconstructed using data from an array of MRI-safe accelerometers, were compared to displacements of neighboring material points in brain tissue, estimated from MRE measurements. Comparison of the relative amplitudes, directions, and temporal phases of harmonic motion in the skulls and brains of six human subjects shows that the skull-brain interface significantly attenuates and delays transmission of motion from skull to brain. In contrast, in a cylindrical gelatin “phantom”, displacements of the rigid case (reconstructed from accelerometer data) were transmitted to the gelatin inside (estimated from MRE data) with little attenuation or phase lag. This quantitative characterization of the skull-brain interface will be valuable in the parameterization and validation of computer models of TBI.

Concepts: Cerebrospinal fluid, Pia mater, Traumatic brain injury, Skull, Dura mater, Arachnoid mater, Meninges, Brain

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Deposition of amyloid-β (Aβ) in the brain parenchyma and vessels is one of the hallmarks of Alzheimer disease (AD). Recent observations of Aβ deposition in iatrogenic Creutzfeldt-Jakob disease (iCJD) after dural grafting or treatment with pituitary extracts raised concerns whether Aβ is capable of transmitting disease as seen in prion diseases by the disease-associated prion protein. To address this issue, we re-sampled and re-evaluated archival material, including the grafted dura mater of two cases with iCJD (28 and 33-years-old) without mutations in the AβPP, PSEN1 and PSEN2 genes, and carrying ε3/ε3 alleles of the APOE gene. In addition, we evaluated 84 dura mater samples obtained at autopsy (mean age 84.9 ± 0.3) in the community-based VITA study for the presence of Aβ deposition. We show that the dura mater may harbor Aβ deposits (13 %) in the form of cerebral amyloid angiopathy or amorphous aggregates. In both iCJD cases, the grafted dura mater had accumulated Aβ. The morphology and distribution pattern of cerebral Aβ deposition together with the lack of tau pathology distinguishes the Aβ proteinopathy in iCJD from AD, from that seen in young individuals without cognitive decline carrying one or two APOE4 alleles, and from that related to traumatic brain injury. Our novel findings of Aβ deposits in the dura mater, including the grafted dura, and the distinct cerebral Aβ distribution in iCJD support the seeding properties of Aβ. However, in contrast to prion diseases, our study suggests that such Aβ seeding is unable to reproduce the full clinicopathological phenotype of AD.

Concepts: Dura mater, Gene, Traumatic brain injury, Cerebral amyloid angiopathy, Brain, Alzheimer's disease, Amyloid, Prion

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Our knowledge on intracranial pain-sensitive structures in humans comes essentially from observations during neurosurgical procedures performed in awake patients. It is currently accepted that intracranial pain-sensitive structures are limited to the dura mater and its feeding vessels and that small cerebral vessels and pia mater are insensitive to pain, which is inconsistent with some neurosurgical observations during awake craniotomy procedures. We prospectively collected observations of painful events evoked by mechanical stimulation (touching, stretching, pressure, or aspiration) of intracranial structures during awake craniotomies, routinely performed for intraoperative functional mapping to tailor brain tumour resection in the eloquent area. Intraoperatively, data concerning the locations of pain-sensitive structures were drawn by the surgeon on a template and their corresponding referred pain was indicated by the patient by drawing a cross on a diagram representing the head. Ninety-three painful events were observed and collected in 53 different patients (mean age 41.2 years, 25 males) operated on awake craniotomy for left (44 cases) or right (nine cases) supra-tentorial tumour resection in eloquent areas. On average, 1.8 painful events were observed per patient (range 1-5). All the painful events were referred ipsilaterally to the stimulus. In all cases, the evoked pain was sharp, intense and brief, stopped immediately after termination of the causing action, and did not interfere with the continuation of the surgery. In 30 events, pain was induced by stimulation of the dura mater of the skull base (23 events) or of the falx (seven events) and was referred predominantly in the V1 territory and in the temporal region. In 61 cases, pain was elicited by mechanical stimulation of the pia mater or small cerebral vessels of the temporal (19 events), frontal (25 events), parietal (four events) lobes and/or the peri-sylvian region, including the insular lobe (13 events), and referred in the V1 territory. In this observational study, we confirmed that dura of the skull base and dura of the falx cerebri are sensitive to pain and that their mechanical stimulation induced pain mainly referred in the sensory territories of the V1 and V3 divisions of the trigeminal nerve. Unlike earlier studies, we observed that the pia and the small cerebral vessels were also pain-sensitive, as their mechanical stimulation induced pain referred mainly in the V1 territory. These observations suggest that small pial cerebral vessels may also be involved in the pathophysiology of primary and secondary headaches.

Concepts: Falx cerebri, Insular cortex, Pain, Skull, Arachnoid mater, Pia mater, Meninges, Dura mater

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OBJECTIVE Small acute epidural hematomas (EDHs) treated conservatively carry a nonmeasurable risk of late enlargement due to middle meningeal artery (MMA) lesions. Patients with EDHs need to stay hospitalized for several days, with neurological supervision and repeated CT scans. In this study, the authors analyzed the safety and efficacy of the embolization of the involved MMA and associated lesions. METHODS The study group consisted of 80 consecutive patients harboring small- to medium-sized EDHs treated by MMA embolization between January 2010 and December 2014. A literature review cohort was used as a control group. RESULTS The causes of head injury were falls, traffic-related accidents (including car, motorcycle, and pedestrian vs vehicle accidents), and assaults. The EDH topography was mainly temporal (lateral or pole). Active contrast leaking from the MMA was seen in 57.5%; arteriovenous fistulas between the MMA and diploic veins were seen in 10%; and MMA pseudoaneurysms were found in 13.6% of the cases. Embolizations were performed under local anesthesia in 80% of the cases, with N-butyl-2-cyanoacrylate, polyvinyl alcohol particles, or gelatin sponge (or a combination of these), obtaining MMA occlusion and complete resolution of the vascular lesions. All patients underwent follow-up CT scans between 1 and 7 days after the embolization. In the 80 cases in this series, no increase in size of the EDH was observed and the clinical evolution was uneventful, without Glasgow Coma Scale score modification after embolization and with no need for surgical evacuation. In contrast, the control cohort from the literature consisted of 471 patients, 82 (17.4%) of whom shifted from conservative treatment to surgical evacuation. CONCLUSIONS This study suggests that MMA embolization is a highly effective and safe method to achieve size stabilization in nonsurgically treated acute EDHs.

Concepts: Glasgow Coma Scale, Polyvinyl alcohol, Surgery, Dura mater, Meninges, Middle meningeal artery

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OBJECTIVES: To examine the extent of brain abnormality in patients with coeliac disease referred for neurological opinion and evaluate MR imaging sequences as biomarkers for neurological dysfunction, given the lack of readily available serological markers of neurological disease in this cohort. METHODS: Retrospective examination of a consecutive cohort of patients (n=33, mean age=44±13 years (range 19-64)) with biopsy proven coeliac disease referred for neurological opinion. Patients were divided into subgroups based on their primary neurological complaint (balance disturbance, headache and sensory loss). 3T MR was used to evaluate differences in brain grey matter density, cerebellar volume, cerebellar neurochemistry and white matter abnormalities (WMAs) between subjects and controls. RESULTS: Cerebellar volume was significantly less in the patient group than in controls (6.9±0.7% vs 7.4±0.9% of total intracranial volume, p<0.05). Significantly less grey matter density was found in multiple brain regions, both above and below the tentorium cerebelli, than in controls (p<0.05). 12 (36%) patients demonstrated WMAs unexpected for the patient's age, with the highest incidence occurring in the headache subgroup. This subgroup averaged almost twice the number of WMAs per MR imaging than the subgroup with balance disturbance and six times more than the subgroup with sensory loss. CONCLUSION: Patients with established coeliac disease referred for neurological opinion show significant brain abnormality on MR imaging. MR imaging may provide valuable biomarkers of disease in this patient cohort.

Concepts: Dura mater, Hospital, Neurology, Cerebellum, Patient, Brain, Neuroanatomy, Central nervous system

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Migraine is one of the most common and most disabling disorders. Between attacks, migraine patients are otherwise normal but are sensitized to non-noxious events known as triggers. The purpose of these studies was to investigate whether a headache-like event causes sensitization, or priming, to subsequent subthreshold events. Interleukin-6 (IL-6) was applied to the rat cranial dura mater which produced cutaneous facial and hindpaw allodynia that lasted 24 hours. At 72-hours, IL-6 treated rats developed allodynia in response to dural stimulation with either a pH 6.8 or pH 7.0 solution and to a systemic nitric oxide (NO) donor, a well-known migraine trigger. Vehicle-treated rats did not respond to either pH stimulus nor to the NO donor, demonstrating that IL-6 exposure primes rats to subthreshold stimuli. Inhibitors of brain-derived neurotrophic factor (BDNF) signaling given either systemically or intracisternally 24-hours after IL-6 eliminated responses to dural pH stimulation at 72 hours. Additionally, intracisternal administration of BDNF without prior dural stimulation produced allodynia and once resolved, animals were primed to dural pH 6.8/pH 7.0 and a systemic NO donor. Finally, hindpaw IL-6 produced paw allodynia but not priming to paw injection of pH 7.0 at 72 hours demonstrating differences in priming depending on location. These data indicate that afferent input from the meninges produces BDNF-dependent priming of the dural nociceptive system. This primed state mimics the interictal period of migraine where attacks can be triggered by normally non-noxious events and suggests that BDNF-dependent plasticity may contribute to migraine.

Concepts: Pia mater, Rat, Neurotrophins, Meninges, Nerve growth factor, Neurotrophin, Brain-derived neurotrophic factor, Dura mater