Positron Emission Tomographic Study of Post-Ischaemic-Hypoxic Amnesia

Abstract

Background: Despite extensive research, it still remains controversial as to what the precise location of the critical lesions underlying amnesia actually is. The amnesic syndrome is believed to be heterogeneous and due to several distinct functional deficits. Patients and Methods: Two patients, a 45-year-old woman and a 56-year-old man, with sudden cardiopulmonary arrest and successful resuscitation, were left with a clear amnesic syndrome as main neurological sequela. During their revalidation period, they underwent a positron emission tomographic (PET) examination, utilizing the ¹³NH₃ bolus technique at rest and after intravenous acetazolamide administration. Results: Both PET studies showed more or less similar features with a decrease in regional cerebral blood flow (rCBF) in the frontal, temporal and parietal lobes. In addition, the rCBF was increased in both thalami of the 45-year-old woman and in the striata of the 56-year-old man. Acetazolamide vasoreactivity was most lost in the frontal lobes. Conclusions: In the present PET study, we demonstrated that destruction of the inhibitory pathways to the thalamus and basal ganglia by ischaemic-hypoxic frontal lesions could be one of the mechanisms leading to amnesia.

Amnesia and Pain Relief after Cardiopulmonary Resuscitation in a Cancer Pain Patient: A Case Report

“…This occurred in the absence of gross cellular damage. In a positron emission tomographic study of 2 post-ischemic-hypoxic amnesia patients, there was destruction of the inhibitory pathways to the thalamus and basal ganglia (8). Amnesia is not related to the duration of cardiac arrest (9).…”