scholarly journals Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

1983 ◽  
Vol 3 (2) ◽  
pp. 246-249 ◽  
Author(s):  
A. Forster ◽  
O. Juge ◽  
D. Morel
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Blood Volume ◽  
Water Soluble ◽  
Increased Intracranial Pressure ◽  
Beneficial Effects ◽  
The Mean

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-C02 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 ± 3.2 to 27.0 ± 5.0 ml 100 g−1 min−1 (x̄ ± SD). At a later session under hypercarbia, CBF was 58.8 ± 4.4 ml 100 g−1 min−1 after administration of placebo, and 49.1 ± 10.2 ml 100 g−1 min−1 after midazolam. The mean of the slopes correlating Paco2 and CBF was significantly steeper with midazolam (2.5 ± 1.2 ml 100 g−1 min−1 mm Hg−1) than with placebo (1.5 ± 0.4 ml 100 g−1 min−1 mm Hg−1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.

The effect of increased intracranial pressure on cerebrovascular hemodynamics

1971 ◽  
Vol 34 (6) ◽  
pp. 760-769 ◽  
Author(s):  
Harry M. Lowell ◽  
Byron M. Bloor
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Transit Time ◽  
Mean Transit Time ◽  
Progressive Decrease ◽  
Increased Intracranial Pressure ◽  
Sagittal Sinus ◽  
The Mean ◽  
Wedge Pressure

✓ Both brain edema (increased water content) and enlargement of the vascular compartment have been implicated as being responsible for intracranial hypertension following trauma. In this study pertinent cerebrovascular hemodynamic parameters have been investigated in states of increased intracranial pressure (ICP) and graded trauma to determine whether cerebral edema or vascular factors are of major importance. Utilizing the monkey-epidural balloon experimental model, continuous measurements of the mean arterial pressure (MABP) , jugular outflow pressure (MJVP), and sagittal sinus wedge pressure (SSWP) were obtained. Shulman's observations that the sagittal sinus wedge pressure accurately reflects the intracranial pressure have been confirmed. The total cerebral blood flow (CBF) and mean transit time (t̄) were determined and the total cerebral blood volume (CBV) computed. From these data the venous (Rv), arterial (Ra), and total resistances (Rt) were calculated. Analysis of these parameters during both the acute elevation of ICP and that following graded trauma has demonstrated: 1) a progressive decrease in the total cerebral blood flow and volume and a concomitant increase in the mean transit time; 2) a progressive increase in the total resistance with a shift from the arterial to the venous side; 3) a progressive decrease in the perfusion pressure (PP = MABP-SSWP); 4) impairment of CO2 reactivity pari passu with vasomotor activity and autoregulation of flow to pressure. The findings did not support the concept that increased intracranial pressure following trauma is the result of an increase in the size of the cerebrovascular compartment.

Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model

1998 ◽  
Vol 274 (5) ◽  
pp. H1715-H1728 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Nonlinear Interaction ◽  
Cerebral Blood Volume ◽  
Cerebral Hemodynamics ◽  
Pial Arteries ◽  
Arterial Circulation ◽  
Neurosurgical Patients

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

Venous sinus stenting shortens the duration of medical therapy for increased intracranial pressure secondary to venous sinus stenosis

2017 ◽  
Vol 10 (3) ◽  
pp. 310-314 ◽  
Author(s):  
Tarek A Shazly ◽  
Ashutosh P Jadhav ◽  
Amin Aghaebrahim ◽  
Andrew F Ducruet ◽  
Brian T Jankowitz ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Medical Therapy ◽  
Venous Sinus ◽  
Increased Intracranial Pressure ◽  
Rnfl Thickness ◽  
Group A ◽  
Sinus Stenosis ◽  
The Mean ◽  
Group B

IntroductionMedical treatment, cerebrospinal fluid (CSF) shunting, and optic nerve sheath fenestration are standard treatments for increased intracranial pressure (ICP) in patients with idiopathic intracranial hypertension (IIH). Venous sinus stenting provides a novel alternative surgical treatment in cases of venous sinus stenosis with elevated ICP.Methods12 consecutive subjects with papilledema, increased ICP, and radiological signs of dural sinus stenosis underwent cerebral venography and manometry. All subjects had papilledema and demonstrated radiological evidence of dural venous sinus stenosis.ResultsSix subjects chose venous stenting (Group A) and six declined and were managed conservatively with oral acetazolamide (Group B). The relative pressure gradient across the venous narrowing was 29±16.3 mm Hg in Group A and 17.6±9.3 mm Hg in Group B (p=0.09). The mean lumbar puncture opening pressure was 40.4±7.6 cm H2O in Group A and 35.6±10.6 cm H2O in Group B (p=0.4). Spectral domain optical coherence tomography (SD-OCT) showed mean average retinal nerve fiber layer (RNFL) thickness of 210±44.8 µm in Group A and 235±124.7 µm in Group B. However, the mean average RNFL thickness at 6 months was 85±9 µm in Group A and 95±24 µm in Group B (p=0.6). The total duration of acetazolamide treatment was 188±209 days in Group A compared with 571±544 days in Group B (p=0.07).ConclusionsIn subjects with venous sinuses stenosis, endovascular stenting offers an effective treatment option for intracranial hypertension which may shorten the duration of medical therapy.

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Metabolic Rate ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Cerebral Perfusion ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Cerebral Metabolic Rate

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).

scholarly journals Cerebral Blood Flow in Low Intracranial Pressure Headaches—What Is Known?

2019 ◽  
Vol 10 (1) ◽  
pp. 2
Author(s):  
Magdalena Nowaczewska ◽  
Henryk Kaźmierczak
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Intracranial Hypotension ◽  
Csf Pressure ◽  
Cerebral Vasodilatation ◽  
The Relationship ◽  
The Brain

Headaches attributed to low cerebrospinal fluid (CSF) pressure are described as orthostatic headaches caused by spontaneous or secondary low CSF pressure or CSF leakages. Regardless of the cause, CFS leaks may lead to intracranial hypotension (IH) and influence cerebral blood flow (CBF). When CSF volume decreases, a compensative increase in intracranial blood volume and cerebral vasodilatation occurs. Sinking of the brain and traction on pain-sensitive structures are thought to be the causes of orthostatic headaches. Although there are many studies concerning CBF during intracranial hypertension, little is known about CBF characteristics during low intracranial pressure. The aim of this review is to examine the relationship between CBF, CSF, and intracranial pressure in headaches assigned to low CSF pressure.

scholarly journals Resection of swollen temporal muscles in patients with intractable intracranial hypertension after decompressive craniectomy

2021 ◽  
Author(s):  
Shih-Hao Huang ◽  
Abel Po-Hao Huang ◽  
Sheng-Jean Huang ◽  
Lu-Ting Kuo
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Decompressive Craniectomy ◽  
Skull Fracture ◽  
Temporal Region ◽  
Brain Swelling ◽  
Increased Intracranial Pressure ◽  
Temporal Muscle ◽  
The Mean

Abstract Background Decompressive craniectomy is employed as treatment for traumatic brain swelling in selected patients. We discussed the effect of temporal muscle resection in patients with intractable intracranial hypertension and temporal muscle swelling after craniectomy. Methods Records of 280 craniectomies performed on 258 patients who were admitted with severe head injury were retrospectively reviewed. Eight patients developed intractable increased intracranial pressure with temporal muscle swelling within 24 h after craniectomy and were treated by muscle resection. Results The initial Glasgow Coma Scale score was 7 ± 1. The mean intracranial pressure was 41.7 ± 8.59 mmHg before muscle resection and 14.81 ± 8.07 mmHg immediately after surgery. Five patients had skull fracture and epidural hematoma at the craniectomy site. The mean intensive care unit stay was 11.25 ± 5.99 days. Glasgow Outcome Scale-Extended scoring performed during the 12-month follow-up visit showed that 6 patients (75%) had a favorable outcome. Conclusions Our study findings indicate that a direct impact on the temporal region during trauma may lead to subsequent temporal muscle swelling. Under certain circumstances, muscle resection can effectively control intracranial pressure.

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