Prophylaxis of postmyelogram headaches

1978 ◽  
Vol 49 (6) ◽  
pp. 869-871 ◽  
Author(s):  
Paul Gutterman ◽  
Honorio S. Bezier
Keyword(s):  
Side Effects ◽  
Control Group ◽  
Content Type ◽  
Fine Print

✓ One hundred patients undergoing myelography received prophylactic autologous epidural blood patches to prevent postmyelogram headache. The results indicate a significant reduction in the incidence and severity of this problem compared to a control group, without any significant side effects.

Prophylaxis of the laminectomy membrane

1978 ◽  
Vol 49 (3) ◽  
pp. 419-424 ◽  
Author(s):  
José Barberá ◽  
José Gonzalez ◽  
José Esquerdo ◽  
Jaime Broseta ◽  
Juan Luis Barcia-Salorio
Keyword(s):  
Side Effects ◽  
Bone Graft ◽  
Periodic Acid ◽  
Scar Tissue ◽  
Control Group ◽  
Periodic Acid Schiff ◽  
Content Type ◽  
Laminectomy Membrane ◽  
Hematoxylin And Eosin ◽  
Fine Print

✓ Sixty laminectomies were performed in dogs to investigate the prevention of the laminectomy membrane and its side effects. These operations were distributed in six groups of 10, one was a control group, and in the others the bone defect was protected with different materials (Oxicel, Silastic, Dacron, methyl methacrylate, and Kiel bone graft). After a survival of 2 months, suboccipital myelography was performed, immediately after which the animals were sacrificed and the operated spinal slice obtained. The different radiographic densities of the tissues of each slice were calculated and the diverse histological nature identified by hematoxylin and eosin, periodic acid Schiff, Masson's trichrome, and Gomori's reticulin stains. Only the acrylic plastic and the Kiel bone graft prevented expansion of the scar tissue inside the spinal canal and adhesions between the dura and the cicatricial overlying muscles. Therefore, the authors suggest that a solid barrier is necessary to effectively prevent the so-called “laminectomy membrane.”

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

Risk of late stroke and survival following carotid endarterectomy procedures for symptomatic patients

1990 ◽  
Vol 73 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Dennis A. Turner ◽  
Jay Tracy ◽  
Stephen J. Haines
Keyword(s):  
Carotid Endarterectomy ◽  
Life Table ◽  
Stroke Risk ◽  
Neurological Symptoms ◽  
Treatment Modalities ◽  
Control Group ◽  
Content Type ◽  
Postoperative Stroke ◽  
Fine Print

✓ The long-term outcome following carotid endarterectomy for neurological symptoms was analyzed using a retrospective life-table approach in 212 patients who had undergone 243 endarterectomy procedures. The postoperative follow-up period averaged 38.9 ± 2.1 months (mean ± standard error of the mean). The endpoints of stroke and death were evaluated in these patients. Patient groups with the preoperative symptoms of amaurosis fugax, transient ischemic attack, and prior recovered stroke were similar in terms of life-table outcome over the follow-up period. Sixty-two percent of symptomatic patients were alive and free of stroke at 5 years. The late risk of stroke (after 30 days postoperatively) averaged 1.7% per year based on a linear approximation to the hazard at each life-table interval (1.3% per year for ipsilateral stroke). The trend of late stroke risk was clearly downward, however, and could be fitted more accurately by an exponential decay function with a half-life of 33 months. Thus, the risk of stroke following carotid endarterectomy for neurological symptoms was highest in the perioperative period, slowly declined with time, and occurred predominantly ipsilateral to the procedure. The definition of a prospective medical control group remains crucial for a critical analysis of treatment modalities following the onset of premonitory neurological symptoms. In the absence of an adequate control group for this series, the calculated perioperative and postoperative stroke risk from this study was compared to data obtained from the literature on stroke risk in medically treated symptomatic patients. This uncontrolled comparison of treatment modalities suggests the combined perioperative and postoperative stroke risk associated with carotid endarterectomy to be modestly improved over medical treatment alone.

Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia

1982 ◽  
Vol 56 (5) ◽  
pp. 706-710 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula
Keyword(s):  
Blood Flow ◽  
Spinal Injury ◽  
Sympathetic Ganglia ◽  
Control Group ◽  
Content Type ◽  
Systemic Pressure ◽  
Sympathetic Regulation ◽  
Mean Systemic Pressure ◽  
Paravertebral Sympathetic Ganglia ◽  
Fine Print

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring. Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls. Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.

Effect of hyperglycemia on brain pH levels in areas of focal incomplete cerebral ischemia in monkeys

1986 ◽  
Vol 65 (5) ◽  
pp. 693-696 ◽  
Author(s):  
W. Richard Marsh ◽  
Robert E. Anderson ◽  
Thoralf M. Sundt
Keyword(s):  
Adverse Effect ◽  
Cerebral Ischemia ◽  
Cell Damage ◽  
Treated Group ◽  
Squirrel Monkeys ◽  
Control Group ◽  
Content Type ◽  
Brain Ph ◽  
Fine Print ◽  
Incomplete Ischemia

✓ The adverse effect of a minimal cerebral blood flow (CBF) in models of global ischemia has been noted by many investigators. One factor believed important in this situation is the level of blood glucose, since a continued supply of this metabolite results in increased tissue lactate, decreased brain pH, and increased cell damage. The authors have extended these observations to a model of focal incomplete ischemia. Brain pH was measured in fasted squirrel monkeys in regions of focal incomplete ischemia after transorbital occlusion of the middle cerebral artery (MCA). In both control and hyperglycemic animals, CBF was reduced to less than 30% of baseline. At 3 hours after MCA occlusion, brain pH in the control group was 6.66 ± 0.68 as compared to 6.27 ± 0.26 in the glucose-treated group. This difference was statistically significant by Student's unpaired t-test (p < 0.05). Thus, hyperglycemia results in decreased tissue pH in regions of focal incomplete cerebral ischemia in monkeys.

Decompressive craniectomy in a rat model of “malignant” cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach

1996 ◽  
Vol 85 (5) ◽  
pp. 853-859 ◽  
Author(s):  
Arnd Doerfler ◽  
Michael Forsting ◽  
Wolfgang Reith ◽  
Christian Staff ◽  
Sabine Heiland ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Decompressive Craniectomy ◽  
Control Group ◽  
Acute Ischemia ◽  
Vessel Occlusion ◽  
Content Type ◽  
Time Points ◽  
Infarction Size ◽  
Mca Occlusion ◽  
Fine Print

✓ Acute ischemia in the complete territory of the carotid artery may lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Although clinical data suggest that patients benefit from undergoing decompressive surgery for acute ischemia, little data about the effect of this procedure on experimental ischemia are available. In this article the authors present results of an experimental study on the effects of decompressive craniectomy performed at various time points after endovascular middle cerebral artery (MCA) occlusion in rats. Focal cerebral ischemia was induced in 68 rats using an endovascular occlusion technique focused on the MCA. Decompressive cranioectomy was performed in 48 animals (in groups of 12 rats each) 4, 12, 24, or 36 hours after vessel occlusion. Twenty animals (control group) were not treated by decompressive craniectomy. The authors used the infarct volume and neurological performance at Day 7 as study endpoints. Although the mortality rate in the untreated group was 35%, none of the animals treated by decompressive craniectomy died (mortality 0%). Neurological behavior was significantly better in all animals treated by decompressive craniectomy, regardless of whether they were treated early or late. Neurological behavior and infarction size were significantly better in animals treated very early by decompressive craniectomy (4 hours) after endovascular MCA occlusion (p < 0.01); surgery performed at later time points did not significantly reduce infarction size. The results suggest that use of decompressive craniectomy in treating cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. By performing decompressive craniectomy neurosurgeons will play a major role in the management of stroke patients.

High titer of interferon (IFN)-neutralizing antibody in a patient with glioblastoma treated with IFN-α

1984 ◽  
Vol 61 (3) ◽  
pp. 591-593 ◽  
Author(s):  
Shin-ichi Otsuka ◽  
Hajime Handa ◽  
Junkoh Yamashita
Keyword(s):  
Side Effects ◽  
Computerized Tomography ◽  
High Titer ◽  
Neutralizing Antibody ◽  
General Malaise ◽  
Content Type ◽  
Long Period ◽  
Site Of Action ◽  
Ifn Therapy ◽  
Fine Print

✓ In a patient with glioblastoma treated with interferon (IFN-α) for a long period of time, a high titer of IFN-neutralizing antibody was detected in the serum during and after IFN therapy. Computerized tomography findings and neurological symptoms in this patient were unchanged during IFN therapy. General malaise, fever, anorexia, nausea, and decrease of leukocytes, platelets, erythrocytes, hemoglobin, and hematocrit were recognized transiently as side effects of IFN administration. These side effects were not serious and resolved spontaneously without discontinuation of therapy. The appearance of IFN-neutralizing antibody is clinically important because the antibody probably neutralizes the effect of systemically administered IFN before it reaches the site of action.

Efficacy of multiple intraarterial papaverine infusions for improvement in cerebral circulation time in patients with recurrent cerebral vasospasm

2004 ◽  
Vol 100 (3) ◽  
pp. 414-421 ◽  
Author(s):  
James K. Liu ◽  
Michael S. Tenner ◽  
Oren N. Gottfried ◽  
Edwin A. Stevens ◽  
Joshua M. Rosenow ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Cerebral Circulation ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Primary Treatment ◽  
Circulation Time ◽  
Control Group ◽  
Content Type ◽  
The Mean ◽  
Cerebral Circulation Time ◽  
Fine Print

Object. Cerebral vasospasm that is caused by aneurysmal subarachnoid hemorrhage and that is refractory to maximal medical management can be treated with selective intraarterial papaverine infusions. The effects of single papaverine treatments on cerebral circulation time are well known. The purpose of this study was to assess the efficacy of multiple, repeated papaverine infusions on the cerebral circulation time in patients with recurrent vasospasm. Methods. A retrospective study was conducted in 17 patients who received multiple intraarterial papaverine infusions in 91 carotid artery (CA) territories for the treatment of cerebral vasospasm. Cerebral circulation times were measured from the first angiographic image, in which peak contrast was seen above the supraclinoid internal CA, to the peak filling of cortical veins. Glasgow Outcome Scale (GOS) scores assessed 12 months after discharge were reviewed. Cerebral circulation times in 16 CA territories were measured in a control group of 11 patients. Seventeen patients received a total of 91 papaverine treatments. Prolonged cerebral circulation times improved after 90 (99%) of 91 papaverine treatments. The prepapaverine mean cerebral circulation time was 6.54 seconds (range 3.35–27 seconds) and the immediate postpapaverine mean cerebral circulation time was 4.19 seconds (range 2.1–12.6 seconds), an overall mean decrease of 2.35 seconds (36%, p < 0.001). Recurrent vasospasm reflected by prolonged cerebral circulation times continued to improve with subsequent papaverine infusions. Repeated infusions were just as successful quantitatively as the primary treatment (mean change 2.06 seconds). The mean cerebral circulation time in the control group was 5.21 seconds (range 4–6.8 seconds). In five patients a dramatic reversal of low-attenuation changes was detected on computerized tomography scans. The mean GOS score at 12 months after discharge was 3.4. Conclusions. The preliminary results indicate that multiple intraarterial papaverine treatments consistently improve cerebral circulation times, even with repeated infusions in cases of recurrent vasospasm.

Calpain-calpastatin system of canine basilar artery in vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Ikuya Yamaura ◽  
Eiichi Tani ◽  
Takaomi C. Saido ◽  
Koichi Suzuki ◽  
Nobutaka Minami ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Early Stage ◽  
Local Application ◽  
Neutral Protease ◽  
Control Group ◽  
Calpain Activity ◽  
Fresh Blood ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, while contraction was induced in the normal canine basilar artery by a local application of KCl or serotonin after transclival exposure. The control animals were injected with saline instead of fresh blood. The activation of μ-calpain, a Ca++-dependent neutral protease, in the basilar artery was studied by evaluating the conversion from its inactivated into its activated form on immunoblots. In addition, the activity of calpastatin, an intrinsic inhibitor of calpain, in the basilar artery was determined by assay. The majority of the μ-calpain was inactivated in the control group. In the spastic group, μ-calpain was generally activated markedly in the early stage of vasospasm and moderately thereafter. The contraction induced by KCl or serotonin application was classified into the early phasic and the later tonic stages; μ-calpain was usually activated in the phasic stage and inactivated in the tonic stage. Calpastatin activity was significantly decreased during vasospasm, whereas it was not significantly changed in KCl- or serotonin-induced contraction. The final activity of μ-calpain results from the balance of μ-calpain and calpastatin. This suggests that μ-calpain activity was enhanced continuously in the spastic group and transiently in the KCl or serotonin group, and that the continuous activation of μ-calpain during vasospasm probably induced more proteolytic changes compared to those in the KCl or serotonin group.

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