scholarly journals Short-Duration Hypothermia after Ischemic Stroke Prevents Delayed Intracranial Pressure Rise

2013 ◽  
Vol 9 (5) ◽  
pp. 553-559 ◽  
Author(s):  
L. A. Murtha ◽  
D. D. McLeod ◽  
S. K. McCann ◽  
D. Pepperall ◽  
S. Chung ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Intracranial Pressure ◽  
Short Duration ◽  
Pressure Rise

Cardiovascular Effects of Acutely Raised Intracranial Pressure

1956 ◽  
Vol 185 (3) ◽  
pp. 510-514 ◽  
Author(s):  
Faith K. Brown
Keyword(s):  
Intracranial Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Cardiovascular Effects ◽  
Dominant Factor ◽  
Raised Intracranial Pressure ◽  
Venous Tone ◽  
Cardiac Stimulation ◽  
Experimental Findings ◽  
Ultimate Nature

Cardiovascular effects of acute elevations of intracranial pressure were studied, with special reference to three questions: a) whether vasoconstriction or cardiac stimulation is primarily responsible for the pressor response to this stimulus; b) whether the ultimate nature of the stimulus is neurogenic or humoral; and c) whether or not changes in venous tone occur in response to ICP elevation. It is concluded from the experimental findings that vasoconstriction was the dominant factor in the response, that the reflex is primarily neurogenic, and that the venomotor system shows an active constriction which accompanies the arterial pressure rise.

scholarly journals Ischemic penumbra as a trigger for intracranial pressure rise – A potential cause for collateral failure and infarct progression?

2016 ◽  
Vol 36 (5) ◽  
pp. 917-927 ◽  
Author(s):  
Daniel J Beard ◽  
Caitlin L Logan ◽  
Damian D McLeod ◽  
Rebecca J Hood ◽  
Debbie Pepperall ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Choroid Plexus ◽  
Pressure Rise ◽  
Ischemic Penumbra ◽  
Stroke Model ◽  
Cellular Processes ◽  
Stroke Models ◽  
Alternate Mechanism ◽  
Anterior Choroidal ◽  
Choroidal Artery

We have recently shown that intracranial pressure (ICP) increases dramatically 24 h after minor intraluminal thread occlusion with reperfusion, independent of edema. Some of the largest ICP rises were observed in rats with the smallest final infarcts. A possible alternate mechanism for this ICP rise is an increase of cerebrospinal fluid (CSF) volume secondary to choroid plexus damage (a known complication of the intraluminal stroke model used). Alternatively, submaximal injury may be needed to induce ICP elevation. Therefore, we aimed to determine (a) if choroid plexus damage contributes to the ICP elevation, (b) if varying the patency of an important internal collateral supply to the middle cerebral artery (MCA), the anterior choroidal artery (AChA), produces different volumes of ischemic penumbra and (c) if presence of ischemic penumbra (submaximal injury) is associated with ICP elevation. We found (a) no association between choroid plexus damage and ICP elevation, (b) animals with a good internal collateral supply through the AChA during MCAo had significantly larger penumbra volumes and (c) ICP elevation at ≈24 h post-stroke only occurred in rats with submaximal injury, shown in two different stroke models. We conclude that active cellular processes within the ischemic penumbra may be required for edema-independent ICP elevation.

scholarly journals Rapid Brain Death following Cardiac Arrest without Intracranial Pressure Rise and Cerebral Circulation Arrest

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Maxime Nguyen ◽  
Thomas Bièvre ◽  
Abdelouaid Nadji ◽  
Bélaïd Bouhemad
Keyword(s):  
Cardiac Arrest ◽  
Intracranial Pressure ◽  
Brain Death ◽  
Unusual Case ◽  
Neuronal Damage ◽  
Pressure Rise ◽  
Electric Activity ◽  
Cellular Toxicity ◽  
Intracranial Pressure Elevation ◽  
Brain Reperfusion

We describe here an unusual case of brain death following cardiac arrest. Brain electric activity had totally ceased, allowing the confirmation of brain death, despite normal cerebral blood flow (assessed by both transcranial doppler and tomodensitometry) and no evidence of intracranial hypertension. In our case, a residual electric activity was assessed at admission and lesions worsened on imaging during ICU stay, suggesting that part of the neuronal damage occurred after brain reperfusion. All these elements suggest BD rather by cellular toxicity than intracranial pressure elevation.

The measurement of intracranial pressure and brain displacement due to short-duration dynamic overpressure loading

Shock Waves ◽  
2017 ◽  
Vol 28 (1) ◽  
pp. 63-83 ◽  
Author(s):  
A. S. Iwaskiw ◽  
K. A. Ott ◽  
R. S. Armiger ◽  
A. C. Wickwire ◽  
V. D. Alphonse ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Short Duration

scholarly journals Exaggerated Postural Blood Pressure Rise Is Related to a Favorable Outcome in Patients With Acute Ischemic Stroke

Stroke ◽  
2012 ◽  
Vol 43 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Marcel J.H. Aries ◽  
Desiree C. Bakker ◽  
Roy E. Stewart ◽  
Jacques De Keyser ◽  
Jan Willem J. Elting ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Pressure Rise ◽  
Favorable Outcome ◽  
Blood Pressure Rise

scholarly journals Intracranial Pressure Elevation after Ischemic Stroke in Rats: Cerebral Edema is Not the Only Cause, and Short-Duration Mild Hypothermia is a Highly Effective Preventive Therapy

2014 ◽  
Vol 35 (4) ◽  
pp. 592-600 ◽  
Author(s):  
Lucy A Murtha ◽  
Damian D McLeod ◽  
Debbie Pepperall ◽  
Sarah K McCann ◽  
Daniel J Beard ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Short Duration ◽  
Cerebral Edema ◽  
Mild Hypothermia ◽  
Dry Weight ◽  
Preventive Therapy ◽  
Stroke Onset ◽  
Experimental Stroke ◽  
Moderate Hypothermia ◽  
Intracranial Pressure Elevation

In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35 °C) or moderate (32.5 °C) hypothermia, or normothermia (37 °C) was induced after stroke onset. Edema was measured in three studies, using wet—dry weight calculations, T2-weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ΔICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset.

Effects of Targeted Temperature Management on Drugs

2019 ◽  
pp. 963-966
Author(s):  
Lauren K. Ng Tucker
Keyword(s):  
Traumatic Brain Injury ◽  
Cardiac Arrest ◽  
Ischemic Stroke ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Bacterial Meningitis ◽  
Cerebral Hemorrhage ◽  
Targeted Temperature Management ◽  
Temperature Management ◽  
The Past

Hypothermia therapy, better known as targeted temperature management (TTM), has increased in popularity in the past several years and has only proven benefits in the setting of cardiac arrest. It has been unsuccessful or not sufficiently proven in traumatic brain injury,bacterial meningitis, cerebral hemorrhage and ischemic stroke. TTM has been shown to decrease intracranial pressure and is used in the management of refractory intracranial pressure despite recent evidence suggesting harm.

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