@article{
 title = {Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: clinicoanatomic correlations.},
 type = {article},
 year = {1986},
 identifiers = {[object Object]},
 pages = {329-33},
 volume = {36},
 websites = {http://www.ncbi.nlm.nih.gov/pubmed/3951698},
 month = {3},
 id = {2e8b5654-0c09-3511-9258-6ad669ebbe72},
 created = {2017-03-07T13:14:27.000Z},
 accessed = {2017-01-07},
 file_attached = {false},
 profile_id = {6c9e6aac-7161-32b3-b6fd-71f53812ce7a},
 group_id = {b5e61a11-29b0-34f4-99cc-f9f2b2c08e68},
 last_modified = {2017-03-07T13:14:28.000Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Hijdra1986},
 abstract = {Fifty-seven of 176 prospectively studied patients with aneurysmal subarachnoid hemorrhage (SAH) developed delayed cerebral ischemia. Clinical features included hemispheric focal signs (13), decrease in level of consciousness (14), or both (30), and mutism (15). Forty-seven patients showed hypodense lesions on CT in one (19) or multiple vascular territories (22), or diffusely in one or both hemispheres (6). Twenty-eight had symmetric decrease in ventricular size. Of 18 autopsied patients, only 1 had a purely univascular lesion. The clinical, CT, and pathologic features suggest that delayed cerebral ischemia after SAH is a multivascular or diffuse process in most patients.},
 bibtype = {article},
 author = {Hijdra, A and Van Gijn, J and Stefanko, S and Van Dongen, K J and Vermeulen, M and Van Crevel, H},
 journal = {Neurology},
 number = {3}
}

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