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Cerebral vasospasm
Salles, Antonio A. F. de;
Arquivos de Neuro-Psiquiatria , 1987, DOI: 10.1590/S0004-282X1987000300014
Abstract: cerebral vasospasm is an important component of pathological entities such as migraine, subarachnoid hemorrhage (sah), head trauma, post cerebral ischemia and/or hypoxia. the mechanisms underlying cerebral vasospasm in these diseases are not completely understood. neurochemical and morphological factors involved in the cerebral circulation control are reviewed in this article. the circulatory changes observed after subarachnoid hemorrhage are taken as a model. it is concluded that multiple biochemical, physiological and morphological factors are involved in the cerebral vascular responses after sah. possible treatment alternatives for cerebral vasospasm based on its etiology are discussed.
VERAPAMIL AND LOPERAMIDE
MANZOOR AHMED UNAR,MAHBOOB AHMED WAGAN,GULSHAN ARA JALBANI,Shaheen Shah
The Professional Medical Journal , 2010,
Abstract: Background: In smooth muscle cells, an increase in cytosolic free calcium concentration is an essential step for the cells tocontract. The increase in calcium concentration occurs by influx from the extra cellular medium through calcium ion channels. Calcium channels have potential role in regulation of motility in gastrointestinal tract so there is growing interest in calcium channel blockers as a potential pharmacological approach to the treatment of various gastrointestinal motor disorders. In this study we evaluate the inhibitory effects of verapamil on spontaneous contractions of isolated guinea pig ileum and compare them with inhibitory effects of loperamide. Materials and Methods: Isolated intestinal segments of sixteen guinea pigs were used in this study. Serial dilutions (10-18 - 10-3 gm/ml) of loperamide and verapamil were administered; effects observed and recorded by 7B Grass Polygraph machine. Results: We observed that at lower concentrations, loperamide showed more inhibitory effects than verapamil while at higher concentrations (10-4 and 10-3 gm/ml) verapamil showed more inhibitory effects than loperamide on the contractions of isolated guinea pig ileum. Conclusion: This study gave us a clue thatverapamil found a potent inhibitor of small intestinal contractions as loperamide. However one can presume further that calcium channel blocker verapamil acting on calcium channel receptor on GIT will be developed with more specific effects on smooth muscle of intestinal tract.
Post-Aneurysmal Subarachnoid Hemorrhage Vasospasm, Clinical Correlation between the Aneurysm Site and Clinical Vasospasm  [PDF]
Ahmed Ali, Mohamed A.R. Soliman
Open Journal of Modern Neurosurgery (OJMN) , 2018, DOI: 10.4236/ojmn.2018.83025
Abstract: Background: Intracranial vasospasm is a common complication following subarachnoid hemorrhage (SAH). The radiographic vasospasm can reach up to 90% of aneurysmal SAH. Materials and Methods: 139 consecutive patients admitted to Cairo University Hospitals from June 2013 to September 2014 with SAH who had been enrolled in a retrospective controlled study were analyzed retrospectively for the occurrence of vasospasm. The data collected from the charts of Cairo University Hospitals were the patient’s demographics, clinical presentation, aneurysm location, treatment modality, and Glasgow Outcome Scale (GOS) scores. We excluded 24 patients with nonaneurysmal SAH, 3 internal carotid artery (ICA) aneurysms, 7 with multiple aneurysms and 4 patients died before treatment. Results: 72 males and 29 females were included in the study, mean age 53.5 ± 11.5 years. Twelve patients had aneurysms located in the vertebral artery group, 24 had middle cerebral artery aneurysms, 11 had pericallosal aneurysms, and 54 patients had anterior communicating artery (ACoA) complex aneurysms. Radiographic vasospasm occurred in 62.4% with the highest incidence (75.9%) at the ACoA complex group. Symptomatic vasospasm occurred in 48.5% with the highest incidence (63%) at the anterior communicating artery complex aneurysm location. The mean GOS at 6 months follow-up was 4.2. The worse GOS was found in the vertebral artery (VA) aneurysm group with a mean of 3.75. Conclusion: Aneurysms of the anterior communicating artery complex group have a greater risk of both radiographic and clinical vasospasm. Also, the worse 6 months follow-up GOS when an aneurysm was located in the VA group.
Quadruple H therapy for vasospasm
Walid M,Zaytseva Nadezhda
Annals of Indian Academy of Neurology , 2009,
Abstract: Triple H therapy has been enthusiastically used to increase cerebral blood flow in cases of vasospasm. Nevertheless, the oxygen-carrying capacity of the blood is lowered with this treatment. This side effect can theoretically be partially corrected using hyperbaric oxygen therapy (HBO) which appears to be the missing ring in the above therapeutic regimen. We conducted a review of of the available evidence regarding the beneficial effects of HBO in preventing postoperative ischemic complications due to vasospasm after surgery on ruptured cerebral aneurysms and the rationale for including HBO into the standards of care of these difficult patients.
Genetics of Cerebral Vasospasm  [PDF]
Travis R. Ladner,Scott L. Zuckerman,J Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/291895
Abstract: Cerebral vasospasm (CV) is a major source of morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH). It is thought that an inflammatory cascade initiated by extravasated blood products precipitates CV, disrupting vascular smooth muscle cell function of major cerebral arteries, leading to vasoconstriction. Mechanisms of CV and modes of therapy are an active area of research. Understanding the genetic basis of CV holds promise for the recognition and treatment for this devastating neurovascular event. In our review, we summarize the most recent research involving key areas within the genetics and vasospasm discussion: (1) Prognostic role of genetics—risk stratification based on gene sequencing, biomarkers, and polymorphisms; (2) Signaling pathways—pinpointing key inflammatory molecules responsible for downstream cellular signaling and altering these mediators to provide therapeutic benefit; and (3) Gene therapy and gene delivery—using viral vectors or novel protein delivery methods to overexpress protective genes in the vasospasm cascade. 1. Introduction Cerebral vasospasm (CV) is the narrowing of the major cerebral arteries following aneurysmal subarachnoid hemorrhage (aSAH) and is a leading contributor to the morbidity and mortality associated with aSAH. The annual incidence of aSAH in the United States is between 21,000 and 33,000 people [1]. Of these, approximately 67% will develop vasospasm [2, 3]. In the setting of aSAH, CV has a biphasic course, with an acute and chronic phase. The acute phase typically begins 3 to 4 hours after hemorrhage, with rapid, spontaneous resolution. In contrast, the chronic phase begins 3 to 5 days later, with maximum narrowing between days 6 and 8, resolving after about 14 days [4]. CV can be diagnosed angiographically or clinically. Angiographic vasospasm refers to the observed narrowing of contrast medium in the major cerebral arteries. Radiologic modalities used to diagnose CV include computed tomography angiography (CTA), magnetic resonance angiography (MRA), and catheter angiography. Clinical vasospasm is the sequelae of neurocognitive deficits presumably as a result of a prolonged ischemic state. Both angiographic and clinical vasospasms can lead to cerebral infarction. Angiographic and clinical vasospasms appear to be distinct phenomena, with aSAH patients presenting with angiographic CV only (43% of patients), both angiographic and clinical CV (33% of patients), or none of them (24% of patients) [5]. Although there are many hypotheses on the pathogenesis of CV, it still remains a poorly understood
Immunologic effects of Verapamil
Moradmand S,Safari F
Tehran University Medical Journal , 1998,
Abstract: Calcium channel blockers are used worldwide in CAD, hypertension and arrhythemia. As recent international studies show these drugs in addition to cardiovascular effects have immunosuppressive effects and can prolong graft life in transplanted patients. In a single blind prospective trial we studied 30 patients on 120 mg/d Verapamil for at least 3 months compared with 15 patients on placebo. Changes of cell immunity markers were impressive as T suppressor lymphocytes increased and CD4/CD8 ratio decreased significantly compared with placebo (P<0.05). This study confirms that Verapamil reduce cell immunity that may prone human beings to infections and on the other side we can use it in hypertensive patients with organ graft.
The Search of the Effects of Verapamil and Papaverin on LIMA Graft Flow in Beating Heart Coronary Bypass  [PDF]
?brahim Sami Karacan,?mer Ulular,Kanat ?z???k,U?ursay K?z?ltepe
Ko?uyolu Kalp Dergisi , 2010,
Abstract: Purpose: The most important problem encountered during the preparation phase of LIMA as being the most important graft which is used in coronary surgery and the same problem after this phase is vasospasm of LIMA. In this study, we evaluated the effects of two vasodilator drugs on LIMA flow which are used on patients in beatingheart coronary artery bypass surgery. Material and Method: 40 patients were investigated who were undergone beating heart coronary artery bypass surgery. Their average age was 61.50± 11.76. The patients were divided in two groups according to applied vasodilatordrugs (papaverin and verapamil groups). The existence of DM, TA and ACT values were recorded during blood flows measurement. The findings: Statistical difference was determined in male patients when compared to female patients (for verapamil p=0.037, for papaverin p=0.042) and in patients with high TA when compared to patients with low TA in the measurements done just before topical drug application and LIMA anastomoses (for verapamil, before drug application p=0.001, after drug application p=0.046, for papaverin before drug application p=0.012, after drug application p=0.021). In both groups, statistically important LIMA blood flow rises were seen after topical drug injection. However papaverin was superior to verapamil when ratio of their ability of increasing blood flow was taken into account (p=0.045). Conclusion: We concluded that short-timed warm bathing process with papaverin increased LIMA blood flow in comparison with the same process done with verapamil; besides, we saw that to keep TA high raises LIMA flow regardless of what kind of vasodilator drugs are used. We claim that, to use papaverin instead of verapamil as topical drug and to keep TA high peroperatively will be beneficial to LIMA flow just after LIMA greft was harvestedin patients undergone beating heart coronary artery bypass surgery.
Cerebral vasospasm after subarachnoid hemorrhage  [PDF]
Milojevi? T.M.,Baljozovi? B.V.,Raki? M.Lj.,Nestorovi? B.D.
Acta Chirurgica Iugoslavica , 2008, DOI: 10.2298/aci0802055m
Abstract: Cerebral vasospasm causes permanent neurolological deficit or death occurrence in 13% of clinical cases. Peak frequency is from 8-10th day after SAH. The purpose of this study is factor analysis that may have influence on vasospasm development , as well as predictor determination. The study is prospective and analysis 192 patients treated in Institute of Neurosurgery, Clinical Centre of Serbia, Belgrade. The majority of patients were admitted in hospital in first four days after SAH, and 184 had GCS over 7. Univariate methods of factor analysis were used, and for significance of predictors influence testing multivariante regression analysis was used . Vasospasm occurred in 22,40% of all cases. No relationships have been found between sex, age, previous hypertension, timing of surgery, appearance of hydrocephalus and intracerebral hematoma, hypertermia or mean arterial blood pressure, with occurrence of cerebral vasospasm. Factors with significantly associated with the occurrence of vasospasm were: hearth disease, hypernatriemia, Hct, clinical grade on admission as well as preoperative clinical grade and Fisher CT scan grade. In the first four days after SAH, Fisher scan grade, preoperative clinical grade and Hct, appeared as predictors. After four days, clinical grade on admission and hypernatiemia, showed as predictors.
Cerebral Vasospasm in Traumatic Brain Injury  [PDF]
Daniel R. Kramer,Jesse L. Winer,B. A. Matthew Pease,Arun P. Amar,William J. Mack
Neurology Research International , 2013, DOI: 10.1155/2013/415813
Abstract: Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%–68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%–16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinical course tends to be milder, although extreme cases may occur. Traumatic vasospasm can occur in the absence of subarachnoid hemorrhage. Surveillance transcranial Doppler ultrasonography (TCD) has been utilized to monitor for radiographic vasospasm following TBI. However, effective treatment modalities remain limited. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be used judiciously in TBI patients, and calcium-channel blockers have offered mixed clinical results. Currently, the paucity of large prospective cohort studies and level-one data limits the ability to form evidence-based recommendations regarding the diagnosis and management of vasospasm associated with TBI. 1. Introduction Traumatic brain injury (TBI) bears a heavy societal burden [1]. With an incidence rate of approximately 1.5 million new cases per year, TBI is the leading cause of death in the USA between the ages of one and forty-five [1]. Primary TBI management focuses on patient stabilization and treatment of elevated intracranial pressure (ICP). Surgical decompression and/or clot evacuation can decrease mass effect and cerebral edema, thus mitigating progressive neurological decline [2, 3]. The frequency of SAH following head trauma is estimated at 39%–65% [4–9], and its presence is an independent predictor of poor functional outcome [4, 7, 10, 11]. Severity of hemorrhage on CT scan has been shown to correlate with clinical status [12]. Although significant morbidity and mortality are attributable to the inciting trauma, deleterious sequelae of secondary injury are considerable and remain a critical focus of medical therapies. Vasospasm is a delayed, secondary consequence that can profoundly impact neurological recovery and functional outcome after TBI. Although vasospasm may result from traumatic subarachnoid hemorrhage (tSAH), other mechanisms such as blast-induced neurotrauma are increasingly recognized as causative factors [13–16]. This paper reviews the epidemiology, diagnosis, pathophysiology, prevention, and treatment of vasospasm
Cerebral Vasospasm Pharmacological Treatment: An Update  [PDF]
Ioannis Siasios,Eftychia Z. Kapsalaki,Kostas N. Fountas
Neurology Research International , 2013, DOI: 10.1155/2013/571328
Abstract: Aneurysmal subarachnoid hemorrhage- (aSAH-) associated vasospasm constitutes a clinicopathological entity, in which reversible vasculopathy, impaired autoregulatory function, and hypovolemia take place, and lead to the reduction of cerebral perfusion and finally ischemia. Cerebral vasospasm begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed for preventing or reversing cerebral vasospasm. Triple “H” therapy, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators, administration of substances like magnesium sulfate, statins, fasudil hydrochloride, erythropoietin, endothelin-1 antagonists, nitric oxide progenitors, and sildenafil, are some of the therapeutic protocols, which are currently employed for managing patients with aSAH. Intense pathophysiological mechanism research has led to the identification of various mediators of cerebral vasospasm, such as endothelium-derived, vascular smooth muscle-derived, proinflammatory mediators, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Oral, intravenous, or intra-arterial administration of antagonists of these mediators has been suggested for treating patients suffering a-SAH vasospam. In our current study, we attempt to summate all the available pharmacological treatment modalities for managing vasospasm. 1. Introduction Aneurysmal subarachnoid hemorrhage (aSAH) constitutes a major cause of stroke, as approximately 3–15% of all stroke cases are due to ruptured intracranial aneurysms [1–4]. Data from population-based studies suggest that the incidence rates vary considerably from 6 to 20 per 100,000 population, with the highest rates reported from Japan and Finland [5–8]. Outcome after aSAH depends on several factors, including the severity of the initial event, the peri-ictal medical management, various surgical variables, and the incidence of aSAH-induced complications. Cerebral vasospasm (CV) is the most frequent and troublesome complication after aSAH. Ecker and Riemenschneider [9] and Robertson [10] were the first ones, who pointed out the occurrence of cerebral arterial spasm following aSAH [9, 10]. Later on, Fisher and his colleagues published a synopsis regarding cerebral vasospasm [11]. Vasospasm, as the term implies, constitutes a reduction in the caliber of a vessel. However, in aSAH cases, the occurrence of vasospasm means much more than just narrowing a cerebral vessel lumen, with significant
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