Acute intracranial hypertension and brain-stem blood flow

1984 ◽  
Vol 60 (3) ◽  
pp. 566-571 ◽  
Author(s):  
Seigo Nagao ◽  
Norio Sunami ◽  
Takumi Tsutsui ◽  
Yutaka Honma ◽  
Fumiyuki Momma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Brain Stem ◽  
Inferior Colliculus ◽  
Medulla Oblongata ◽  
Systemic Arterial Pressure ◽  
Content Type ◽  
Cushing Response ◽  
The Mean ◽  
Mass Lesions

✓ This study has been carried out to evaluate the effect of supratentorial mass lesions on the local cerebral blood flow (CBF) of the brain stem. Local CBF of the thalamus, inferior colliculus, and medulla oblongata, and supra- and infratentorial pressure were serially measured in 52 cats with intracranial hypertension produced by supratentorial balloon expansion. The mean control local CBF's in the thalamus, inferior colliculus, and medulla oblongata were 37.5, 42.1, and 30.7 ml/100 gm/min, respectively. At 20 to 30 mm Hg of supratentorial pressure, the local CBF of the thalamus started to decrease, and at 20 mm Hg of infratentorial pressure, the local CBF of the inferior colliculus began to decrease. Finally, at 40 to 60 mm Hg of infratentorial pressure, the local CBF of the medulla oblongata was affected. At the beginning of uncal herniation, indicated by anisocoria, the mean local CBF of the inferior colliculus abruptly decreased from 33.7 to 19.6 ml/100 gm/min in 16 cats. The Cushing response was evoked at a mean supratentorial pressure of 93.4 mm Hg and infratentorial pressure of 49.9 mm Hg in 16 cats. When the systemic arterial pressure was increased to the highest level in 13 cats, the mean local CBF of the medulla oblongata did not show significant change (a decrease from 22.8 to 20.9 ml/100 gm/min). The results suggest that at the beginning of uncal herniation, the local CBF of the upper brain stem markedly decreased. During the Cushing response, the local CBF of the medulla oblongata did not change significantly.

Acute regional cerebral blood flow changes caused by severe head injuries

1991 ◽  
Vol 74 (3) ◽  
pp. 407-414 ◽  
Author(s):  
Donald W. Marion ◽  
Joseph Darby ◽  
Howard Yonas
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Brain Stem ◽  
Head Injuries ◽  
Clinical Signs ◽  
Content Type ◽  
Tomography Method ◽  
Gcs Score ◽  
Mass Lesions

✓ To evaluate the changes in cerebral blood flow (CBF) that occur immediately after head injury and the effects of different posttraumatic lesions on CBF, 61 CBF studies were obtained using the xenon-computerized tomography method in 32 severely head-injured adults (Glasgow Coma Scale score (GCS) ≤ 7). The measurements were made within 7 days after injury, 43% in the first 24 hours. During the 1st day, patients with an initial GCS score of 3 or 4 and no surgical mass had significantly lower flows than did those with a higher GCS score or mass lesions (p < 0.05): in the first 1 to 4 hours, those without surgical mass lesions had a mean CBF of 27 cc/100 gm/min, which rose to 44 cc/100 gm/min by 24 hours. Patients without surgical mass lesions who died tended to have a lower global CBF than did those with better outcomes. Mass lesions were associated with a high global CBF and bihemispheric contusions with the lowest flows. By 24 hours after injury, global blood flow increased in groups that originally had low flows and decreased in those with very high initial flows, such that by 36 to 48 hours, most patients had CBF values between 32 and 55 cc/100 gm/min. Lobar, basal ganglion, and brain-stem blood flow values frequently differed by 25% or more from global averages. Brain-stem CBF varied the most but did not correlate with clinical signs of brain-stem dysfunction. Double studies were performed at two different pCO2 values in 10 patients with various posttraumatic lesions, and the CO2 vasoresponsivity was calculated. Abnormal CO2 vasoresponsivity was found with acute subdural hematomas and defuse cerebral swelling but not with epidural hematomas. In patients without surgical mass lesions, the findings suggest that CBF in the first few hours after injury is often low, followed by a hyperemic phase that peaks at 24 hours. Global CBF values vary widely depending on the type of traumatic brain injury, and brain-stem flow is often not accurately reflected by global CBF values. These findings underscore the need to define regional CBF abnormalities in victims of severe head injury if treatment is intended to prevent regional ischemia.

Experimental neurogenic pulmonary edema

1981 ◽  
Vol 54 (5) ◽  
pp. 627-631 ◽  
Author(s):  
Julian T. Hoff ◽  
Merry Nishimura ◽  
Jose Garcia-Uria ◽  
Sandra Miranda
Keyword(s):  
Pulmonary Edema ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Systemic Arterial Hypertension ◽  
Cushing Response ◽  
Intraventricular Infusion ◽  
Sympathetic Discharge

✓ Neurogenic pulmonary edema (NPE) was produced consistently in normal cats by increasing intracranial pressure with an intraventricular infusion of mock cerebrospinal fluid. The usual elevation of systemic arterial pressure (SAP) that follows severe intracranial hypertension (the “Cushing response”) was controlled by blood withdrawal at variable rates to achieve and maintain constant cerebral perfusion pressure (CPP) in three groups of cats of 50, 20, and 0 mm Hg, respectively, for 30 minutes. In this model, NPE occurs in the absence of increased SAP and in the presence of decreasing CPP. These results indicate that systemic arterial hypertension is not an essential stimulus for the development of NPE, and suggest that the lungs are directly affected by the intense sympathetic discharge evoked by severe intracranial hypertension.

Catecholamine response to a gradual increase of intracranial pressure

1993 ◽  
Vol 79 (5) ◽  
pp. 705-709 ◽  
Author(s):  
Johan van Loon ◽  
Bharati Shivalkar ◽  
Chris Plets ◽  
Jan Goffin ◽  
T. Budya Tjandra-Maga ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Gradual Increase ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Catecholamine Response ◽  
Cushing Response ◽  
The Mean ◽  
The Brain

✓ To determine the catecholamine response to progressive intracranial hypertension, intracranial pressure (ICP) was raised gradually by continuous expansion of an epidural balloon in seven dogs. Hemodynamic parameters, ICP, and cerebral perfusion pressure (CPP) were monitored continuously and serum catecholamine levels began to rise when CPP was in the low-positive range (20 to 30 mm Hg), reaching a peak just after brain death (CPP ≤ 0 mm Hg). There was no correlation between ICP and the catecholamine peak. Compared to control values, the mean increase was 286-fold for epinephrine and 78-fold for norepinephrine. Temporally, the catecholamine peak corresponded well with the observed hemodynamic changes. These results suggest that ischemia in certain parts of the brain stem is responsible for the hemodynamic changes observed in intracranial hypertension (such as the Cushing response), and they show that catecholamines play an important role in these hemodynamic changes.

Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions

1978 ◽  
Vol 48 (3) ◽  
pp. 329-331 ◽  
Author(s):  
James E. Cottrell ◽  
Katie Patel ◽  
Herman Turndorf ◽  
Joseph Ransohoff
Keyword(s):  
Intracranial Pressure ◽  
Sodium Nitroprusside ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Intracranial Tumors ◽  
Cerebral Blood Vessels ◽  
Content Type ◽  
The Mean ◽  
Pressure Changes ◽  
Mass Lesions

✓ Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 ± 1.85 to 27.61 ± 3.33 torr (p > 0.0005) and cerebral perfusion pressure decreased from 89.32 ± 3.5 to 43.23 ± 4.60 torr (p < 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.

Pressure in the sagittal sinus during intracranial hypertension in man

1974 ◽  
Vol 40 (5) ◽  
pp. 603-608 ◽  
Author(s):  
Albert N. Martins ◽  
Arthur I. Kobrine ◽  
Douglas F. Larsen
Keyword(s):  
Brain Tumors ◽  
Intracranial Hypertension ◽  
Cerebral Blood Volume ◽  
Content Type ◽  
Sagittal Sinus ◽  
Sagittal Sinus Pressure ◽  
The Mean ◽  
The Difference ◽  
Spatial Compensation ◽  
Sinus Pressure

✓ Intracranial pressure (ICP) and sagittal sinus pressure (SSP) were measured simultaneously in 12 patients with brain tumors and secondary intracranial hypertension (ICH). In nine, the mean SSP was largely unaffected by changes in ICP. In three, SSP changed with the ICP. In all but one patient, the ICP remained higher than SSP and, as the ICP increased, the difference between the two also increased. Sinograms performed during ICH demonstrated partial collapse of the sinuses in some patients and not in others. The mean SSP in adults with brain tumors appears to respond unpredictably to changes in ICP. Since the rate of cerebrospinal fluid drainage depends upon the gradient between ICP and SSP, intracranial spatial compensation is probably influenced by the response of SSP to ICP. Individuals with gradients that rapidly increase because their sinuses do not collapse probably compensate more rapidly than those whose sinuses do collapse. This assumed difference in the rate of spatial compensation may account for some of the variability of the ICP response to an enlarging intracranial mass or a change in cerebral blood volume.

Effect on the Cushing response of different rates of expansion of a supratentorial mass

1978 ◽  
Vol 49 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Abdul Hamid Zidan ◽  
John P. Girvin
Keyword(s):  
Heart Rate ◽  
Full Range ◽  
Blood Gases ◽  
Systemic Arterial Pressure ◽  
Critical Volume ◽  
Experimental Conditions ◽  
Content Type ◽  
Cerebral Dysfunction ◽  
Cushing Response ◽  
Supratentorial Mass

✓ The effects on the three components (respiration, blood pressure, and heart rate) of the Cushing response (CR) were studied in cats by the continuous expansion of a supratentorial balloon. The rate of expansion was varied over the range of 0.006 to 0.6 ml/min, during which systemic arterial pressure, heart rate, respiratory rate, and blood gases were monitored. For the different rates the time the CR took to develop, and the balloon volume required for that development were measured. The final volume (“critical volume”) for eliciting the CR was more or less constant over the full range of rates of infusion (balloon expansion), a fact that supports the Monro-Kellie doctrine. This constancy of critical volume (CCV) gives rise to a highly statistically significant relationship between the rate of infusion and the latency to the production of the CR, and it is described by a power curve. Thus the development of cerebral dysfunction under these experimental conditions is independent of the rate of expansion and only dependent upon this critical volume. Exceptions to this concept of a critical volume, at the extreme of rates of expansion of lesions in patients, are predicted.

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

1983 ◽  
Vol 59 (6) ◽  
pp. 938-944 ◽  
Author(s):  
Quentin J. Durward ◽  
A. Lorne Amacher ◽  
Rolando F. Del Maestro ◽  
William J. Sibbald
Keyword(s):  
Cardiac Output ◽  
Intracranial Hypertension ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Optimum Level ◽  
Moderate Degree ◽  
Content Type ◽  
Arterial Oxygen Content ◽  
Head Elevation ◽  
The Mean

✓ To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15°, 30°, and 60°. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15° (a fall of −4.5 ± 1.6 mm Hg, p < 0.001) and 30° (a fall of −6.1 ± 3.5 mm Hg, p < 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60°, the mean ICP increased to −3.8 ± 9.3 mm Hg of baseline, while the CPP decreased −7.9 ± 9.3 mm Hg (p < 0.02), and the cardiac index also fell −0.25 ± 0.28 liters/min/sq m (p < 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15° or 30°) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0°) or higher (60°) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Cerebral cysticercosis with aqueductal obstruction

1980 ◽  
Vol 53 (2) ◽  
pp. 252-255 ◽  
Author(s):  
Tung Pui Poon ◽  
Edward J. Arida ◽  
Wolodymyr P. Tyschenko
Keyword(s):  
Intracranial Hypertension ◽  
Brain Stem ◽  
Normal Pressure Hydrocephalus ◽  
Signs And Symptoms ◽  
Normal Pressure ◽  
Content Type ◽  
Neurological Signs ◽  
Cerebral Cysticercosis ◽  
The Brain ◽  
Fine Print

✓ The authors report a case of cerebral cysticercosis which presented with generalized nonspecific neurological signs and symptoms attributed to acute aqueductal obstruction, with concomitant intracranial hypertension. These were characteristic intracranial calcifications along with angiographically demonstrated signs of hydrocephalus. Contrast encephalography clearly demonstrated aqueductal obstruction. Pathologically, the aqueductal obstruction was shown to be due to parasitic invasion of the brain stem with compression of the aqueduct. The presence of typical intracranial calcification in conjunction with either obstructive or normal-pressure hydrocephalus should alert the observer to the possibility of cerebral cysticercosis.

Intraoperative identification of motor areas of the rhomboid fossa using direct stimulation

1993 ◽  
Vol 79 (3) ◽  
pp. 393-399 ◽  
Author(s):  
Christian Strauss ◽  
Johann Romstöck ◽  
Christopher Nimsky ◽  
Rudolf Fahlbusch
Keyword(s):  
Brain Stem ◽  
Fourth Ventricle ◽  
Complete Removal ◽  
Direct Stimulation ◽  
Content Type ◽  
Rhomboid Fossa ◽  
Stem Lesions ◽  
Mass Lesions ◽  
The Brain ◽  
Motor Areas

✓ Intraoperative electrical identification of motor areas within the floor of the fourth ventricle was successfully carried out in a series of 10 patients with intrinsic pontine lesions and lesions infiltrating the brain stem. Direct electrical stimulation was used to identify the facial colliculus and the hypoglossal triangle before the brain stem was entered. Multichannel electromyographic recordings documented selective stimulation effects. The surgical approach to the brain stem was varied according to the electrical localization of these structures. During removal of the lesion, functional integrity was monitored by intermittent stimulation. In lesions infiltrating the floor of the fourth ventricle, stimulation facilitated complete removal. Permanent postoperative morbidity of facial or hypoglossal nerve dysfunction was not observed. Mapping of the floor of the fourth ventricle identifies important surface structures and offers a safe corridor through intact nervous structures during surgery of brain-stem lesions. Reliable identification is particularly important in mass lesions with displacement of normal topographical anatomy.

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