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Books on the topic 'Arachnoïde'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Arachnoid Cysts. Elsevier, 2018. http://dx.doi.org/10.1016/c2015-0-07024-1.

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Arachnoid Cysts. Elsevier, 2018. http://dx.doi.org/10.1016/c2017-0-01879-7.

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3

Eslick, Guy D., Knut Wester, and Helland A. Christian. Arachnoid Cysts: Epidemiology, Biology, and Neuroimaging. Elsevier Science & Technology Books, 2017.

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4

Wester, Knut. Arachnoid Cysts: Clinical and Surgical Management. Elsevier Science & Technology Books, 2017.

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5

Nguyen, Katherine. Arachnoid Cysts: Epidemiology, Treatment and Clinical Outcomes. Nova Science Publishers, Incorporated, 2016.

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6

British Brain & Spine Foundation., ed. Sub-arachnoid haemorrhage: A guide for patients and carers. 2nd ed. London: British Brain and Spine Foundation, 1998.

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7

Rizk, Elias, Aaron S. Dumont, Joe Iwanaga, Shane R. Tubbs, and Anthony V. D'Antoni. Cerebrospinal Fluid and Arachnoid Space : Volume 1: Clinical Anatomy and Physiology. Academic Press, 2021.

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8

British Brain and Spine Foundation. and Royal College of Surgeons of England., eds. The British Brain and Spine Foundation sub-arachnoid haemorrhage information booklet. London: Royal College of Surgeons of England, 1994.

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9

Publications, ICON Health. Arachnoid Cysts - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. Icon Health Publications, 2004.

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10

Publications, ICON Health. The Official Patient's Sourcebook on Arachnoid Cysts: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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11

Vodopivec, Ivana, and Tracey A. Cho. Neurobiology of Transverse Myelitis and Infectious Myelopathies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0153.

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Infectious agents cause spinal cord pathology by three different mechanisms: direct invasion/infection of neural tissues (i.e., infective myelitis), secondary inflammation and tissue bystander damage with or without autoimmune pathogenesis (parainfectious myelitis), or involvement of extra-axial structures (including the pia-arachnoid, the dura, the epidural space, or the adjacent spinal bones or intervertebral discs), resulting in compressive or ischemic myelopathy. This chapter describes the pathogenesis and treatment of these disorders.

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12

Taylor, Jennie, and Patrick Y. Wen. Meningomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0130.

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Meningiomas are the most common primary brain tumor diagnosed in adults. Arising from the arachnoid (meningothelial) cells of the inner layer of the dura, they are often slow growing, but can lead to significant morbidity. They can invade through the outer layer of dura into overlying bone or skin, or into critical bordering structures such as the cavernous sinus or orbits, or encase cerebral blood vessels. These limitations can make surgical resection difficult if not impossible in some circumstance. However, they rarely metastasize outside the central nervous system (CNS), with the lungs being the most common site seen with higher-grade tumors.

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13

Chamberlain, Marc C., Stephanie E. Combs, and Soichiro Shibui. Neoplastic meningitis: metastases to the leptomeninges and cerebrospinal fluid. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0021.

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Carcinomatous meningitis or meningeal carcinomatosis is a term that defines leptomeningeal metastases arising as a result of metastases from systemic solid cancers. Similarly, lymphomatous and leukaemic meningitis result from cerebrospinal fluid dissemination of lymphoma or leukaemia. All three entities are commonly referred to as neoplastic meningitis or leptomeningeal metastases due to involvement of both the cerebrospinal fluid compartment as well as the leptomeninges comprised of the pia and arachnoid. Treatment options are limited for these neurological complications and outcomes are generally poor. New therapeutic strategies are desperately needed as more cancer patients survive longer and are at increased risk for neoplastic meningitis.

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14

Buchanan, Ian A., and Gabriel Zada. Rathke’s Cleft Cysts. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0017.

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Cystic lesions involving the sella have a distinct differential diagnosis including Rathke cleft cyst, cystic pituitary adenoma, craniopharyngioma, arachnoid cyst, and epidermoid among other entities. Workup includes not only cranial imaging but also endocrine evaluation for pituitary dysfunction and ophthalmologic evaluation to assess for visual deficits that may not be immediately apparent to the patient at presentation. Rathke cleft cysts are common and may be found in 20% of autopsy specimens. However, symptomatic Rathke cleft cysts are rare, and surgical decisions should be made judiciously based on preoperative symptoms and workup. Endonasal transphenoidal approach for cyst fenestration is a common surgical management technique for symptomatic lesions. Complete resection of the Rathke cleft cyst wall is not required.

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15

Paech, Michael J., and Patchareya Nivatpumin. Postdural puncture headache. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0027.

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Postdural puncture headache (PDPH) may follow either deliberate or unintentional (accidental) penetration of the interdigitating meninges, the dura and arachnoid mater. It is one of the most common and clinically important complications of regional anaesthesia and analgesia in the obstetric population. The headache develops as a consequence of cerebrospinal fluid loss, low intracranial pressure and cerebrovascular changes in the upright position and can prove debilitating. The diagnosis is clinical, making thorough assessment and regular review all the more important, to revise treatment plans, exclude rare serious pathology such as subdural haematoma, and avoid misdiagnosis. This chapter reviews the pathophysiology, incidence, risk factors (needle, technical and patient related), features, natural history, diagnosis, and management of PDPH. High level evidence supports prevention by using small gauge, non-cutting spinal needles, but other preventative strategies against either unintentional dural puncture or PDPH are poorly supported. The absent or poor efficacy of measures such as bed rest, hydration, cerebral vasoconstrictor therapy, epidural or intrathecal saline injection, intrathecal catheter placement or prophylactic epidural blood patch, is noted. Validation of better evidence supporting epidural morphine or intravenous cosyntropin is required. Symptomatic treatment of PDPH is also unreliable. Very limited evidence that requires substantiation supports a modest benefit from caffeine, gabapentinoids or intravenous hydrocortisone. The intervention of epidural blood patch is highly likely to relieve post-spinal PDPH, but only completely resolves epidural needle-induced PDPH in 30–50% of cases. Much detail about EBP remains undetermined, but delayed intervention and injection of approximately 20 mL of autologous blood appear appropriate.

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