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  • Journal of Neurosurgery: Pediatrics x
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Susanne Guhl, Michael Kirsch, Heinz Lauffer, Michael Fritsch and Henry W. S. Schroeder

complications caused by compression of cerebral and neural structures, typically by the draining collector, are seen. In the majority of cases, however, flow-related complications due to an imbalance between in- and outflow in the DVA system have been described. 11 In most symptomatic DVAs, an association with other vascular malformations such as cavernous malformations was found. 12 Rare mechanical complications are as follows: 1) hydrocephalus by compression of the aqueduct; 9 , 13 or 2) neurovascular compression of cranial nerves inducing trigeminal neuralgia, facial

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Aqueel Pabaney, Shawn L. Hervey-Jumper, Joseph Domino, Cormac O. Maher and Lynda J. S. Yang

resulting from vascular compression of the cranial nerves is a well-known phenomenon. Trigeminal neuralgia is the most well-studied neurovascular compression syndrome. 1 , 5 , 6 Pain from trigeminal neuralgia is thought to result from focal demyelination in the region of compression and ectopic generation of spontaneous impulses and their ephaptic spread due to close apposition of those demyelinated axons. 7 Decompression of the nerve root leads to rapid relief and has been explained by the separation of demyelinated axons, remyelination, and the recovery of nerve

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Nader S. Dahdaleh and Arnold H. Menezes

, 16–18 The pathophysiology of this facial pain syndrome in patients with CM-I is explained by chronic extrinsic compression of the tonsils on the lateral medulla and a resulting effect on the spinal trigeminal tracts that mediate the face's sensitivity to pain and temperature. 14 In cases of associated syringobulbia and -myelia, intrinsic compression on these tracts may also be a contributing factor. 9 An alternative hypothesis can be made that in patients with trigeminal neuralgia associated with CM, general crowding of the posterior fossa causes neurovascular

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Jennifer Hong, Jared M. Pisapia, Zarina S. Ali, Austin J. Heuer, Erin Alexander, Gregory G. Heuer and Eric L. Zager

T horacic outlet syndrome (TOS) is a neurovascular compression syndrome caused by constriction of the brachial plexus or subclavian artery and vein as they exit the thoracic outlet. This syndrome can have a variable presentation, and symptoms are typically divided into vascular or neurogenic, although an individual may have a mixture of both. Neurogenic TOS (nTOS) has a wide constellation of symptoms including pain, paresthesias, and motor deficits in the neck and/or extremity. 26 The diagnosis of TOS is controversial, because the definition describes the

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Zhe Guan, Todd Hollon, J. Nicole Bentley and Hugh J. L. Garton

related to neurovascular compression or recurrent cyst rupture should be offered surgical intervention. In patients with normal neurological function and no signs of raised intracranial pressure, conservative management with close observation may be recommended initially. Because ECs grow slowly, this approach can make surgery unnecessary or delay surgery by several years. 7 As these lesions are poorly responsive to chemotherapy and radiation, excision remains the definitive treatment. 6 Ideally, gross-total resection is performed to minimize the risk of tumor

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Doris D. Wang, Kenneth W. Martin, Kurtis I. Auguste and Peter P. Sun

cranial nerves as well as cerebellopontine angle lesions. 13 , 19 Balanced SSFP is also useful in detecting neurovascular compression of the trigeminal nerve. 12 However, bSSFP and other traditional MRI techniques are limited by their susceptibility to motion artifacts caused by heartbeat, breathing, or swallowing. While bSSFP is effective at detecting detailed structures within the CSF space, dynamic thin membranous adhesions are difficult to visualize using a non time-resolved approach since they move synchronously with CSF pulsations. 7 , 16 A c ardiac gated