anatomic location and density of trigeminal innervations at
the circle of Willis (4,12). Other proposed pathophysiological
mechanisms include virus spread via the bloodstream
or the cerebrospinal fluid; immune mediated vascular
reaction secondary to distant infection (3,12); sympathetic
stimulation due to the local irritant effect of the chickenpox
lesions in the region of the superior cervical ganglion (12);
thrombotic vascular occlusion by virus mediated direct
endotelial damage (1,12); and acquired transient deficiencies
of protein S and/or protein C (1,6,8).
Data from the literature review suggest that PVCA
usually affects young, otherwise healthy children, within
anatomic location and density of trigeminal innervations atthe circle of Willis (4,12). Other proposed pathophysiologicalmechanisms include virus spread via the bloodstreamor the cerebrospinal fluid; immune mediated vascularreaction secondary to distant infection (3,12); sympatheticstimulation due to the local irritant effect of the chickenpoxlesions in the region of the superior cervical ganglion (12);thrombotic vascular occlusion by virus mediated directendotelial damage (1,12); and acquired transient deficienciesof protein S and/or protein C (1,6,8).Data from the literature review suggest that PVCAusually affects young, otherwise healthy children, within
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