Early Spasm Research Articles

Comparison of transposition and interposition methods in microvascular decompression for hemifacial spasm: an analysis of 109 cases performed by a single surgeon in a single-center retrospective study

BackgroundMicrovascular decompression (MVD), the standard surgical approach for hemifacial spasm (HFS), can be divided into the interposition and transposition methods. Although the risk of HFS recurrence following interposition has been reported, there is limited data comparing long-term outcomes between both methods performed by a single surgeon. This study aimed to investigate the efficacy of MVD techniques on HFS by comparing surgical outcomes performed by a single surgeon in a single-center setting.MethodsA total of 109 patients who underwent MVD were analyzed and divided into the transposition (86 patients) and interposition (23 patients) groups. Postoperative outcomes at 1 month and 1 year were assessed and compared, including rates of spasm relief, complications, and recurrence.ResultsOutcome assessment revealed higher rates of early spasm relief in the interposition group (66.3% vs. 100%, transposition vs. interposition, respectively, p = 0.0004), although spasm relief at 1-year postoperatively was comparable between the two groups (84.9% vs. 95.7%, transposition vs. interposition, respectively, p = 0.2929). No significant differences were observed in complication and recurrence rates. Kaplan–Meier analysis demonstrated no significant differences in the duration of spasm resolution by MVD method (p = 0.4347, log-rank test).ConclusionThis study shows that both the transposition (Surgicel® and fibrin glue) and interposition (sponge) methods were excellent surgical techniques. The interposition method may achieve earlier spasm resolution compared to the transposition method.

Quality of life at 6 years in children treated for West syndrome with hormonal therapy

IntroductionWest syndrome is a severe epileptic encephalopathy occurring in infancy. Majority of affected children suffer from poor epilepsy control in later life and are dependent on care-givers for daily living. There is no previous study evaluating the Quality of Life (QOL) in children suffered from WS. MethodA prospective cohort study was performed at six years in a group of children with West syndrome, followed up in the Sri Lanka Infantile Spasm Study (SLISS). The quality of life was evaluated using Sri Lankan Health-Related Quality-of-Life Index for school children (SLHRQ-S), an age-specific, primary caregiver proxy-rated, validated questionnaire for Sri Lankan children with epilepsy. Information on epilepsy, medication, and daily activities was obtained from the parents. ResultsFifty parents of initial 97 children treated for WS participated. The majority had no ongoing epilepsy (56%) at time of evaluation. The mean QOL was 67.22 (SD 15.68). Mean QOL scores for individual domains showed that physical domain was the worst affected (58.51 (SD = 22.11)). Psychological and social function domains were 68.73 (SD = 17.74) and 75.2 (SD = 14.87), respectively. Male sex (0.02), using multiple anti-seizure medications (0.00) and lower ILAE epilepsy control scale (0.02) were significantly associated with a poor quality of life. Age at onset, delay in treatment, and early spasm control were among the factors that did not influence quality of life. ConclusionDespite having control of their epilepsy in the majority, these children suffered from poor quality of life. The greater impact on the physical domain possibly is related to the effect of underlying pathologies.

The radial artery as a coronary bypass conduit: dealing with hyperreactivity

The radial artery as a coronary bypass conduit: dealing with hyperreactivity

Protective Effect of Spinal Cord Stimulation on Experimental Early Cerebral Vasospasm

In this study we investigate the effects of cervical spinal cord stimulation (cSCS) on experimental ‘early spasm’ in rabbits as described in personal previous experience (Acta Neurochir 2001;143:177–185). Twenty-four adult red Burgundy rabbits wearing a cervical epidural electrode underwent cerebral blood flow (CBF) and functional monitoring of early basilar spasm before and during cSCS. CBF changes, as a consequence of cSCS, occurred in 20 control animals. No CBF changes, consistent with no basilar artery vasospasm, occurred after subarachnoid haemorrhage (SAH) up to the end of the experiments in all the stimulated animals. The role of reversible functional sympathectomy in mediating the effect of spinal cord stimulation on early spasm is discussed. cSCS is able to prevent ‘early spasm’ due to SAH in all the animals studied, independently from the occurrence and the sign of stimulation induced CBF variations.

Spinal cord stimulation and early experimental cerebral spasm: the "functional monitoring" and the "preventing effect".

Clinical and experimental data on cerebral blood flow (CBF) changes during spinal cord stimulation (SCS) were published since 1986. The aims of the present work are: 1. To find an experimental model of reliable, simple and in vivo monitoring of "early" basilar artery spasm after subarachnoid haemorrhage (SAH) and 2. To investigate the effects of cervical spinal cord stimulation (CSCS) on it. Vasospasm due to SAH is both "acute" and "recurrent". Early spasm occurs within minutes of the SAH. its duration is approximately 1 hour. The need of different morphological and haemodynamic methods to evaluate experimental early spasm is reported. To overcome intracranial surgical manipulations and biological effects of contrast and fixation media we designed a model that allows "in vivo" functional monitoring of basilar blood flow far away from the spasm without direct surgical and chemical interference. Subsequently we investigated the effects of CSCS on the new model of "functional monitoring" of the "early" cerebral vasospasm. 29 adult Burgundy rabbits were studied. Group 1: under homeostatic monitoring, "on-line" carotid blood flow (carotid BF) changes produced by SAH in cisterna magna of 12 (plus 5 sham treated) animals were studied from the common carotid artery after external carotid artery occlusion before, during SAH and up to the end of the experiments. All the animals underwent digital subtraction cerebral panangiography (CPA) after SAH obtaining a significant increase of carotid BF only when basilar vasospasm was shown by CPA. Carotid BF increase during basilar vasospasm was defined "functional monitoring" of early spasm. Group 2: Twelve animals wearing a cervical epidural electrode underwent carotid BF "functional monitoring" of early basilar spasm before and during CSCS. Carotid BF changes during CSCS occurred in 10 animals. No carotid BF changes (i.e. no basilar vasospasm) occurred after SAH up to the end of the experiments in all the stimulated animals. CSCS is able to prevent "early spasm" due to SAH in all the animals studied with the new model of "functional monitoring" described, independently from the occurence and the sign for stimulation-induced carotid BF variations. The role and the limits of reversible functional sympathectomy in mediating the effect of CSCS on early vasospam are discussed.

Cisternal talc injection in dog can induce delayed and prolonged arterial constriction resembling cerebral vasospasm morphologically and pharmacologically

The possible role of inflammation in the pathogenesis of cerebral vasospasm has been noted in recent studies. In order to examine the role of inflammation, we examined the vasocontractile activity of talc, which is known to cause severe inflammation, using a canine cisternal talc injection model. Under general anesthesia, a sterile talc powder suspended in saline was injected into the cisterna magna of the dog. Serial vertebral angiography and postmortem histologic changes of the harvested basilar artery were examined. The morphologic and pharmacologic features of talc-induced vessel spasm were compared with the usual autologous blood-induced artery spasm. Cisternal injection of sterile talc powder caused no early spasm, but induced definite basilar arterial constriction 2 days after injection. This vascular constriction was observed to continue up to 7 days after injection. Ultrastructural study of the constricted vessel revealed several morphologic changes, such as corrugation of the elastic lamina, subintimal proliferation, migration of smooth muscle cells, detachment of endothelial cells, etc.; findings that are compatible with the changes observed in vasospasm. Pharmacologic study showed a moderate decrease in the maximal contraction to KCl and UTP. Endothelium-dependent relaxation was markedly disturbed, while endothelium-independent relaxation was preserved. These pharmacologic properties were also similar to those reported in vasospasm. Our present study indicates that the several changes of vascular properties, which had been considered to be specific to cerebral vasospasm, can be regarded as a nonspecific biologic defense reaction against the foreign body. The analysis of the common pathway from talc and autologous blood to vasospasm may lead to the pathogenesis of cerebral vasospasm.

<I>Red Blood Cells are Essential for Late Vasospasm Following Experimentally Induced Subarachnoid Hemorrhage in Dogs</I>

The in vivo spasmogenic activity of various blood components was examined in dogs. Each blood fraction was injected into the cisterna magna at 0.5 or 1.0 ml/kg body weight, after the removal of 0.5 ml/kg body weight of cerebrospinal fluid, and vertebral angiography was then performed. Whole blood induced both early and late arterial spasm. Platelet-rich and platelet-poor plasma produced only early spasm, and no arterial narrowing was observed on days 1, 3, and 7 after injection. On the contrary, intracisternal injection of washed red blood cells (0.5 ml/kg body weight) produced no arterial narrowing for 6 hours after injection and induced moderate arterial narrowing on days 1, 3, and 7 after injection. Hemolysate (a 10-gm/dl concentration of hemoglobin) produced prolonged monophasic arterial narrowing after injection. These results imply that red blood cells are required for late, prolonged arterial narrowing after experimental subarachnoid hemorrhage.

Impairement of vascular reactivity and changes in intracellular calcium and calmodulin levels of smooth muscle cells in canine basilar arteries after subarachnoid hemorrhage.

We examined vascular reactivity to various vasoconstrictors and dilators, and the changes in calcium-calmodulin levels in canine basilar arteries after subarachnoid hemorrhage (SAH). Contractile responses to noradrenaline, serotonin, and potassium chloride were markedly attenuated at 48 hours (P less than 0.05), and further attenuated at 7 and 14 days after SAH (P less than 0.01). Dilation responses to calcium antagonist were maintained at 48 hours after SAH, but were markedly reduced at 7 and 14 days after SAH (P less than 0.05). Transmission electron micrographs of the basilar artery showed contraction of the media between 48 hours and 7 days and degeneration of smooth muscle cells over the 7 days after SAH. Electron microscopic cytochemical examination for calcium showed that intracellular deposits of calcium pyroantimonate increased in smooth muscle cells of basilar arteries at 1 hour after the first intracisternal injection of blood (early spasm), but decreased in smooth muscle cells at 48 hours after SAH (at the beginning of delayed vasospasm). They decreased further in the vessels 7 days after SAH. The calmodulin contents in the basilar arteries were decreased slightly at 6 hours, and significantly (P less than 0.05) at 48 hours after SAH, as determined by radioimmunoassay and phosphodiesterase assay. Therefore, it is considered that delayed vasospasm is not simply an active contraction of the vessels, but a functional or structural derangement of contractile elements of smooth muscle cells after 48 hours after SAH.

Experimental evaluation of the beneficial effect of an antioxidant on cerebral vasospasm.

Based on the previously suggested hypothesis that generation of free radicals leading to lipid peroxidation is involved in the genesis of vasospasm following SAH, the therapeutic effect of an antioxidant on experimental vasospasm was examined. As an antioxidant suitable for this purpose, AVS(1,2-bis(nicotinamide)-propane) was used. Experimental SAH was induced in dogs by intracisternal injection of blood and subsequent changes in the basilar artery diameter was evaluated by angiography. First, intrathecal administration of AVS 3 days after SAH caused prompt resolution of pre-existing chronic vasospasm for 3-4 h. Next, the effect of continuous intravenous administration of saline (control) or AVS was started and continued for 4 days. In the control group, early and chronic spasm was observed on the daily angiography. In the AVS-treated group, early spasm was only moderately inhibited, but the occurrence of chronic spasm was remarkably suppressed in a dose-dependent manner. In these experiments, no adverse effect of AVS on the neurological or systemic conditions was observed. The data indicate that AVS may be beneficial in the treatment of vasospasm following SAH, thereby reinforcing the concept that generation of free radicals is involved in the genesis of vasospasm.

Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581

The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate) was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581. Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs. The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.

Vasospasmogenic substance produced following subarachnoid hemorrhage, and its fate (author's transl)

Whether a patient who has had unfortunate subarachnoid hemorrhage can lead a useful life or even survive is greatly influenced by cerebral vasospasm. We have conducted studies on vasoconstrictive substances developing after subarachnoid hemorrhage and also the possibilities of inactivating drugs as a treatment for vasospasm. Fresh blood and a supernate of the blood-CSF mixture incubated for 1 to 16 days were applied to the basilar artery of adult cats which were exposed by transcervical-transclival approach. After each application, the diameter of the artery was observed and the degree of constriction was measured using a surgical microscope. Constriction due to the application of fresh blood was about 30%, and recovery was observed shortly after. It seems that serotonin isolated from platelet participates greatly in the transient vasoconstriction induced by fresh blood, and that the early spasm clinically is caused by serotonin and mechanical stimulation. Supernate of blood-CSF mixture, incubated for 3 days, has weak activity compared to the powerful (50%) and long lasting activity of those incubated for 7 days. Furthermore, same mixture incubated for 15 days has little or no activity. This change in the vasoconstrictive activity is similar and coincides chronologically with the appearance of late spasm as reported in clinical studies by Suzuki in 19754). Vasogenic substance in 7th day mixtures were investigated. Heat coagulation and ultrafiltration indicates that the vasogenic substance is a protein with a molecular weight exceeding 10, 000. Sephadex G-100 gel chromatography and disc electrophoresis indicates that the substance is hemoglobin. Spectrophotography ensures that this Hb is oxyHb. On the other hand, in 15th day mixtures, oxyHb is converted to metHb. Experimentally, pure metHb has no vasoconstrictive activity. From the result of the present study, it is possible that bleeding from ruptured aneurysm stops spontaneously due to immediate coagulation and early spasm induced by serotonin and mechanical stimulation. Gradually oxyHb is excreted following the hemolysis. The oxyHb volume reaches its peak near or on the 7th day following the bleeding. During this progression, vasospasm is provoked when the oxyHb reaches a responsible volume. From the 7th day following the hemorrhage, oxyHb gradually changes into metHb. By the 15th day all oxyHb had been converted. Subsequently, the metHb is broken into heroin and globin and is absorbed into the blood. We have succeeded in oxidizing oxyHb into metHb with sodium nitrite, thus preventing experimental vasospasm. In the future we intend to continue work with sodium nitrite and other drugs to seek methods to prevent clinical vasospasm.

Experimental cerebral vasospasm

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.