Cerebral blood flow and temporal lobe epileptogenicity

1997 ◽  
Vol 86 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Martin E. Weinand ◽  
L. Philip Carter ◽  
Waleed F. El-Saadany ◽  
Panayiotis J. Sioutos ◽  
David M. Labiner ◽  
...  

✓ Long-term surface cerebral blood flow (CBF) monitoring was performed to test the hypothesis that temporal lobe epileptogenicity is a function of epileptic cortical perfusion. Forty-three bitemporal 2-hour periictal CBF studies were performed in 13 patients. Homotopic regions of temporal cortex maintained interictal epileptic cortical hypoperfusion and nonepileptic normal cortical CBF. At 10 minutes preictus, a statistically significant, sustained increase in CBF was detected on the epileptic temporal lobe. Two minutes preictus, there was approximation of CBF in the epileptic and nonepileptic temporal lobes. Thereafter, electrocorticographic (ECoG) and clinical seizure onset occurred. The linear relationship between CBF in the two hemispheres (epileptic and nonepileptic) was the inverse of normal (y = −0.347x + 62.767, r = 0.470, df = 95, p < 0.05). The data indicated a direct linear correlation between epileptic cortical CBF and seizure interval (frequency−1), a clinical measure of epileptogenicity (r = 0.610, df = 49, p < 0.05). Epileptogenicity was also found to be a logarithmic function of the difference between nonepileptic and epileptic cortical perfusion (r = 0.564, df = 58, t = 5.20, p < 0.05). The results showed that progressive hypoperfusion of the epileptic focus correlated with a decreased seizure interval (increased epileptogenicity). Increased perfusion of the epileptic focus correlated with an increased seizure interval (decreased epileptogenicity). The fact that CBF alterations precede ECoG seizure activity suggests that vasomotor changes may produce electrical and clinical seizure onset.

1996 ◽  
Vol 1 (5) ◽  
pp. E5 ◽  
Author(s):  
Martin E. Weinand ◽  
L. Philip Carter ◽  
Waleed F. El-Saadany ◽  
Panayiotis J. Sioutos ◽  
David M. Labiner ◽  
...  

Long-term surface cerebral blood flow (CBF) monitoring was performed to test the hypothesis that temporal lobe epileptogenicity is a function of epileptic cortical perfusion. Forty-three bitemporal 2-hour periictal CBF studies were performed in 13 patients. Homotopic regions of temporal cortex maintained interictal epileptic cortical hypoperfusion and nonepileptic normal cortical CBF. At 10 minutes preictus, a statistically significant, sustained increase in CBF was detected on the epileptic temporal lobe. Two minutes preictus, there was approximation of CBF in the epileptic and nonepileptic temporal lobes. Thereafter, electrocorticographic (ECoG) and clinical seizure onset occurred. The linear relationship between CBF in the two hemispheres (epileptic and nonepileptic) was the inverse of normal (y = -0.347x + 62.767, r = 0.470, df = 95, p < 0.05). The data indicated a direct linear correlation between epileptic cortical CBF and seizure interval (frequency-1), a clinical measure of epileptogenicity (r = 0.610, df = 49, p < 0.05). Epileptogenicity was also found to be a logarithmic function of the difference between nonepileptic and epileptic cortical perfusion (r = 0.564, df = 58, t = 5.20, p < 0.05). The results showed that progressive hypoperfusion of the epileptic focus correlated with a decreased seizure interval (increased epileptogenicity). Increased perfusion of the epileptic focus correlated with an increased seizure interval (decreased epileptogenicity). The fact that CBF alterations precede ECoG seizure activity suggests that vasomotor changes may produce electrical and clinical seizure onset.


2007 ◽  
Vol 7 (4) ◽  
pp. 91-94 ◽  
Author(s):  
Theodore H. Schwartz

Hemodynamic surrogates of epileptic activity are being used to map epileptic foci with PET, SPECT, and fMRI. However, there are few studies of neurovascular coupling in epilepsy. Recent data indicate that cerebral blood flow, although focally increased at the onset of a seizure, may be temporarily inadequate to meet the metabolic demands of both interictal and ictal epileptic events. Transient focal tissue hypoxia and hyperperfusion may be excellent markers for the epileptic focus and may even precede the onset of the ictal event.


1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.


2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.


2000 ◽  
Vol 92 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Seiji Yamamoto ◽  
Weiyu Teng ◽  
Shigeru Nishizawa ◽  
Takeharu Kakiuchi ◽  
Hideo Tsukada

Object. The hydroxyl radical scavenger (±)-N,N′-propylenedinicotinamide (AVS) has been shown to ameliorate the occurrence of vasospasm following experimental subarachnoid hemorrhage (SAH) and to reduce the incidence of delayed ischemic neurological deficits (DINDs) in patients with SAH. The authors investigated whether prophylactic administration of AVS could improve cerebral blood flow (CBF) and cerebral glucose utilization (CGU) following SAH in rats.Methods. Anesthetized rats were subjected to intracisternal injection of blood (SAH group) or saline (control group). Either AVS (1 mg/kg/min) or saline (vehicle group) was continuously injected into the rat femoral vein. Forty-eight hours later, positron emission tomography scanning was used with the tracers 15O-H2O and 18F-2-fluoro-d-glucose to analyze quantitatively CBF and CGU, respectively, in the frontoparietal and occipital regions (12 regions of interest/group).In SAH rats receiving only vehicle, CBF decreased significantly (p < 0.05, Tukey's test) and CGU tended to decrease, compared with values obtained in control (non-SAH) rats receiving vehicle. In rats that were subjected to SAH, administration of AVS significantly (p < 0.05, Tukey's test) improved CBF and CGU in both the frontoparietal and occipital regions compared with administration of vehicle alone.Conclusions. Prophylactic administration of AVS improves CBF and CGU in the rat brain subjected to SAH, and can be a good pharmacological treatment for the prevention of DINDs following SAH.


1984 ◽  
Vol 60 (5) ◽  
pp. 916-922 ◽  
Author(s):  
Bruce Mickey ◽  
Sissel Vorstrup ◽  
Bo Voldby ◽  
Helle Lindewald ◽  
Aage Harmsen ◽  
...  

✓ A noninvasive three-dimensional method for measuring cerebral blood flow (CBF), xenon-133 inhalation and emission computerized tomography, was used to investigate the CBF changes accompanying delayed neurological deterioration following subarachnoid hemorrhage (SAH). A total of 67 measurements were performed on 20 patients in Hunt and Hess' clinical Grades I to III in the first 21 days post SAH. Five patients with normal CBF tomograms on admission developed delayed neurological deficits in the 2nd week after hemorrhage, at which time repeat CBF tomograms in four patients revealed large areas of well defined regional flow decrease in the vascular territories of the anterior or middle cerebral arteries. Severe vasospasm was noted in three of these patients in whom arteriography was performed in the 2nd week post SAH. Diffuse bihemispheric CBF decreases were noted later in the course of delayed neurological deficits; however, measurements obtained soon after the onset of focal symptoms suggest that the only CBF decreases directly produced by vasospasm in Grade III patients are regional changes.


1996 ◽  
Vol 85 (5) ◽  
pp. 871-876 ◽  
Author(s):  
Mark R. McLaughlin ◽  
Donald W. Marion

✓ There is increasing evidence that regional ischemia plays a major role in secondary brain injury. Although the cortex underlying subdural hematomas seems particularly vulnerable to ischemia, little is known about the adequacy of cerebral blood flow (CBF) or the vasoresponsivity within the vascular bed of contusions. The authors used the xenon-enhanced computerized tomography (CT) CBF technique to define the CBF and vasoresponsivity of contusions, pericontusional parenchyma, and the remainder of the brain 24 to 48 hours after severe closed head injury in 10 patients: six patients with one contusion and four with two contusions, defined as mixed or high-density lesions on CT scanning. The CBF within the contusions (29.3 ± 16.4 ml/100 g/minute, mean ± standard deviation) was significantly lower than both that found in the adjacent 1-cm perimeter of normal-appearing tissue (42.5 ± 15.8 ml/100 g/minute) and the mean global CBF (52.5 ± 17.5 ml/100 g/minute) (p < 0.004, repeated-measures analysis of variance). A subset of seven patients (10 contusions) also underwent a second Xe-CT CBF study during mild hyperventilation (a PaCO of 24–32 mm Hg). In only two of these 10 contusions was vasoresponsivity less than 1% (range 0%–7.6%); in the rim of normal-appearing pericontusional tissue, it was 0.4% to 9.1%. The authors conclude that CBF within intracerebral contusions is highly variable and is often above 18 ml/100 g/minute, the reported threshold for irreversible ischemia. Intracontusional CBF is significantly reduced relative to surrounding brain parenchyma, and CO2 vasoresponsivity is usually present. In the contusion and the surrounding parenchyma, vasoresponsivity may be nearly three times normal, suggesting hypersensitivity to hyperventilation therapy. Given this possible hypersensitivity and relative hypoperfusion within and around cerebral contusions, these lesions are particularly vulnerable to secondary injury such as that which may be caused by hypotension or aggressive hyperventilation.


1998 ◽  
Vol 89 (6) ◽  
pp. 962-970 ◽  
Author(s):  
Theodore H. Schwartz ◽  
Orrin Devinsky ◽  
Werner Doyle ◽  
Kenneth Perrine

Object. Although it is known that 5 to 10% of patients have language areas anterior to the rolandic cortex, many surgeons still perform standard anterior temporal lobectomies for epilepsy of mesial onset and report minimal long-term dysphasia. The authors examined the importance of language mapping before anterior temporal lobectomy. Methods. The authors mapped naming, reading, and speech arrest in a series of 67 patients via stimulation of long-term implanted subdural grids before resective epilepsy surgery and correlated the presence of language areas in the anterior temporal lobe with preoperative demographic and neuropsychometric data. Naming (p < 0.03) and reading (p < 0.05) errors were more common than speech arrest in patients undergoing surgery in the anterior temporal lobe. In the approximate region of a standard anterior temporal lobectomy, including 2.5 cm of the superior temporal gyrus and 4.5 cm of both the middle and inferior temporal gyrus, the authors identified language areas in 14.5% of patients tested. Between 1.5 and 3.5 cm from the temporal tip, patients who had seizure onset before 6 years of age had more naming (p < 0.02) and reading (p < 0.01) areas than those in whom seizure onset occurred after age 6 years. Patients with a verbal intelligence quotient (IQ) lower than 90 had more naming (p < 0.05) and reading (p < 0.02) areas than those with an IQ higher than 90. Finally, patients who were either left handed or right hemisphere memory dominant had more naming (p < 0.05) and reading (p < 0.02) areas than right-handed patients with bilateral or left hemisphere memory lateralization. Postoperative neuropsychometric testing showed a trend toward a greater decline in naming ability in patients who were least likely to have anterior language areas, that is, those with higher verbal IQ and later seizure onset. Conclusions. Preoperative identification of markers of left hemisphere damage, such as early seizure onset, poor verbal IQ, left handedness, and right hemisphere memory dominance should alert neurosurgeons to the possibility of encountering essential language areas in the anterior temporal lobe (1.5–3.5 cm from the temporal tip). Naming and reading tasks are required to identify these areas. Whether removal of these areas necessarily induces long-term impairment in verbal abilities is unknown; however, in patients with a low verbal IQ and early seizure onset, these areas appear to be less critical for language processing.


1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.


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