Perfusion computed tomography thresholds defining ischemic penumbra and infarct core: studies in a rat stroke model.

BACKGROUND: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stroke and guide reperfusion therapies. AIMS: The study aims to determine whether there are important changes in perfusion computed tomography thresholds defining ischemic penumbra and infarct core over time following stroke. METHODS: Permanent middle cerebral artery occlusion was performed in adult outbred Wistar rats (n = 6) and serial perfusion computed tomography scans were taken every 30 mins for 2 h. To define infarction thresholds at 1 h and 2 h post-stroke, separate groups of rats underwent 1 h (n = 6) and 2 h (n = 6) of middle cerebral artery occlusion followed by reperfusion. Infarct volumes were defined by histology at 24 h. Co-registration with perfusion computed tomography maps (cerebral blood flow, cerebral blood volume, and mean transit time) permitted pixel-based analysis of thresholds defining infarction, using receiver operating characteristic curves. RESULTS: Relative cerebral blood flow was the perfusion computed tomography parameter that most accurately predicted penumbra (area under the curve = 0.698) and also infarct core (area under the curve = 0.750). A relative cerebral blood flow threshold of < 75% of mean contralateral cerebral blood flow most accurately predicted penumbral tissue at 0.5 h (area under the curve = 0.660), 1 h (area under the curve = 0.659), 1.5 h (area under the curve = 0.636), and 2 h (area under the curve = 0.664) after stroke onset. A relative cerebral blood flow threshold of < 55% of mean contralateral most accurately predicted infarct core at 1 h (area under the curve = 0.765) and at 2 h (area under the curve = 0.689) after middle cerebral artery occlusion. CONCLUSIONS: The data provide perfusion computed tomography defined relative cerebral blood flow thresholds for infarct core and ischemic penumbra within the first two hours after experimental stroke in rats. These thresholds were shown to be stable to define the volume of infarct core and penumbra within this time window.

Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise.

BACKGROUND: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Therapeutic hypothermia improves outcome after cardiac arrest, is strongly neuroprotective in experimental stroke, and is under clinical trial in stroke. Hypothermia lowers elevated intracranial pressure; however, rebound intracranial pressure elevation and neurological deterioration may occur during rewarming. HYPOTHESES: (1) Intracranial pressure increases 24 h after moderate and small strokes. (2) Short-duration hypothermia-rewarming, instituted before intracranial pressure elevation, prevents this 24 h intracranial pressure elevation. METHODS: Long-Evans rats with two hour middle cerebral artery occlusion or outbred Wistar rats with three hour middle cerebral artery occlusion had intracranial pressure measured at baseline and 24 h. Wistars were randomized to 2·5 h hypothermia (32·5°C) or normothermia, commencing 1 h after stroke. RESULTS: In Long-Evans rats (n = 5), intracranial pressure increased from 10·9 ± 4·6 mmHg at baseline to 32·4 ± 11·4 mmHg at 24 h, infarct volume was 84·3 ± 15·9 mm(3) . In normothermic Wistars (n = 10), intracranial pressure increased from 6·7 ± 2·3 mmHg to 31·6 ± 9·3 mmHg, infarct volume was 31·3 ± 18·4 mm(3) . In hypothermia-treated Wistars (n = 10), 24 h intracranial pressure did not increase (7·0 ± 2·8 mmHg, P < 0·001 vs. normothermia), and infarct volume was smaller (15·4 ± 11·8 mm(3) , P < 0·05). CONCLUSIONS: We saw major intracranial pressure elevation 24 h after stroke in two rat strains, even after small strokes. Short-duration hypothermia prevented the intracranial pressure rise, an effect sustained for at least 18 h after rewarming. The findings have potentially important implications for design of future clinical trials.

Self-administered isoflurane in labour. A comparative study with Entonox.

Entonox (50% nitrous oxide in oxygen) and isoflurane (0.75% in oxygen) were compared as analgesics in the first stage of labour in 32 consenting women. The drugs were self-administered and given in random sequence, each during five consecutive uterine contractions. Each patient acted as her own control. Linear analogue pain scores were significantly lower (p less than 0.001) with isoflurane than with Entonox, but scores for drowsiness were higher for isoflurane. Further study is needed to assess the effects of more prolonged use of isoflurane in labour.

Continuous infusion epidural analgesia in obstetrics. A comparison of 0.08% and 0.25% bupivacaine.

The effects of 0.08% (Group A) and 0.25% (Group B) solutions of bupivacaine were compared in a random manner, to assess continuous pump infusion epidural analgesia in labour. Both solutions were infused at a dose rate of 20 mg bupivacaine/hour. The results in all the mothers who had received infusions lasting more than 4 hours were studied. There were 25 in Group A and 28 in Group B. Any treatment during the infusion epidural for inadequate analgesia, hypotension, etc., was recorded as an intervention. The mean of the intervention-free intervals was significantly greater in Group A than in Group B, and significantly fewer top-up injections were required in Group A. The results show that the administration of a 0.08% solution of bupivacaine into the epidural space by continuous pump infusion is more labour saving than the infusion of a 0.25% solution. The concept that a greater volume infusion rate maintains a more extended liquid sleeve of local anaesthetic in the epidural space is supported.