A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after high-flow bypass for a carotid intracavernous aneurysm
Tekijät: Iihara K, Okawa M, Hishikawa T, Yamada N, Fukushima K, Iida H, Miyamoto S
Kustantaja: AMER ASSOC NEUROLOGICAL SURGEONS
Julkaisuvuosi: 2010
Journal: Journal of Neurosurgery
Tietokannassa oleva lehden nimi: JOURNAL OF NEUROSURGERY
Lehden akronyymi: J NEUROSURG
Vuosikerta: 112
Numero: 6
Aloitussivu: 1254
Lopetussivu: 1259
Sivujen määrä: 6
ISSN: 0022-3085
DOI: https://doi.org/10.3171/2009.9.JNS09345
Tiivistelmä
The authors report a rare case of slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after radial artery/external carotid artery middle cerebral artery bypass graft surgery for an intracavernous carotid artery aneurysm. Under barbiturate protection, a 69-year-old man underwent high-flow bypass surgery combined with carotid artery sacrifice for a symptomatic intracavernous aneurysm. The patient became restless postoperatively, and this restlessness peaked on postoperative Day (POD) 7. Diffusion-weighted and FLAIR MR images obtained on PODs 1 and 7 revealed subtle cortical hyperintensity in the temporal cortex subjected to temporary occlusion. On POD 13, (123)I-iomazenil ((123)I-IMZ) SPECT clearly showed increased distribution on the early image and mildly decreased binding on the delayed image with count ratios of the affected unaffected corresponding regions of interest of 1.23 and 0.84, respectively, suggesting postischemic hyperperfusion. This was consistent with the finding on (123)I-iodoamphetamine SPECT. Of note, neuronal density in the affected cortex on the delayed (123)I-IMZ image further decreased to the affected/unaffected ratio of 0.44 on POD 55 during the subacute stage when characteristic cortical hyperintensity on T1-weighted MR imaging, typical of cortical laminar necrosis, was emerging. The affected cortex showed marked atrophy 8 months after the operation despite complete neurological recovery. This report illustrates, for the first time, dynamic neuroradiological correlations between slowly progressive neuronal death shown by (123)I-IMZ SPECT and cortical laminar necrosis on MR imaging in human stroke. (DOI: 10.3171/2009.9.JNS09345)
The authors report a rare case of slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after radial artery/external carotid artery middle cerebral artery bypass graft surgery for an intracavernous carotid artery aneurysm. Under barbiturate protection, a 69-year-old man underwent high-flow bypass surgery combined with carotid artery sacrifice for a symptomatic intracavernous aneurysm. The patient became restless postoperatively, and this restlessness peaked on postoperative Day (POD) 7. Diffusion-weighted and FLAIR MR images obtained on PODs 1 and 7 revealed subtle cortical hyperintensity in the temporal cortex subjected to temporary occlusion. On POD 13, (123)I-iomazenil ((123)I-IMZ) SPECT clearly showed increased distribution on the early image and mildly decreased binding on the delayed image with count ratios of the affected unaffected corresponding regions of interest of 1.23 and 0.84, respectively, suggesting postischemic hyperperfusion. This was consistent with the finding on (123)I-iodoamphetamine SPECT. Of note, neuronal density in the affected cortex on the delayed (123)I-IMZ image further decreased to the affected/unaffected ratio of 0.44 on POD 55 during the subacute stage when characteristic cortical hyperintensity on T1-weighted MR imaging, typical of cortical laminar necrosis, was emerging. The affected cortex showed marked atrophy 8 months after the operation despite complete neurological recovery. This report illustrates, for the first time, dynamic neuroradiological correlations between slowly progressive neuronal death shown by (123)I-IMZ SPECT and cortical laminar necrosis on MR imaging in human stroke. (DOI: 10.3171/2009.9.JNS09345)
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