A case of posterior reversible encephalopathy syndrome caused by hyperperfusion after carotid endarterectomy

Endo, Tohru; Niwa, Ryoko; Kunii, Naoto; Matsuhashi, Ako; Ishikawa, Osamu; Nakatomi, Hirofumi; Saito, Nobuhito

doi:10.3995/jstroke.10747

Cited by 1 publication

(1 citation statement)

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“…[1,12,18] In the field of neurosurgery, PRES has been reported to occur in cases associated with the treatment for SAH, [11] subsequent shunt placement for normal pressure hydrocephalus (NPH), [13] or hyperperfusion syndrome associated with surgical treatment for internal carotid artery stenosis. [4,8] On average, approximately 40% of all patients diagnosed with PRES require intensive care monitoring and treatment due to severe complications such as epilepsy attack, cerebral ischemia, intracranial hemorrhage, or increased intracranial pressure. [10] However, there have been no randomized controlled trials focusing on the treatment, which should be considered when discussing epidemiological data, diagnostic criteria, and treatment recommendations.…”

Section: Discussionmentioning

confidence: 99%

Asymmetric posterior reversible encephalopathy syndrome secondary to epilepsy occurring in the chronic phase of subarachnoid hemorrhage

Matsumoto¹,

Hanayama²,

Matsumoto³

et al. 2022

Surgical Neurology International

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Background: Posterior reversible encephalopathy syndrome (PRES) is a rare clinical syndrome that refers to a disorder with reversible subcortical vasogenic brain edema involving the parieto-occipital lobe, temporal lobe, basal ganglia, and its surroundings. Radiologically, it is characterized by symmetrical lesions; however, atypical findings have sometimes been reported. Case Description: A 79-year-old woman experienced subarachnoid hemorrhage (SAH) a year and a half previously before this hospitalization. She presented with sudden-onset coma, dacryorrhea, and moderate right hemiparesis and was taken to our hospital. Computed tomography showed no apparent abnormal acute lesions. Electroencephalography confirmed periodic lateralized epileptiform discharges in the left hemisphere. First, based on the findings, she was diagnosed with nonconvulsive status epilepticus and started antiepileptic therapy. Six days after admission, however, multiple asymmetric lesions were confirmed on magnetic resonance imaging. Considering that findings subsequently improved, we finally diagnosed her with asymmetric PRES secondary to epilepsy occurring in the chronic phase of SAH. Aphasia and right hemispatial neglect persisted as sequelae and she was transferred to a rehabilitation hospital with a modified Rankin scale of 3. Conclusion: Excessive elevation of blood flow in the hemisphere is inferred to lead to blood–brain barrier collapse and subsequent asymmetric PRES.

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