Asghar and collaborators35 examined the diameter of extracranial

Asghar and collaborators35 examined the diameter of extracranial and intracranial vessels in subjects suffering from migraine without aura, seeking to avoid a premature dismissal of vascular mechanisms. A novel high-resolution direct MRA imaging technique was used to measure arterial circumference of the extracranial

MMA and the intracranial middle cerebral artery (MCA). The study found dilation of both MMA and MCA during migraine attack. Sumatriptan administration caused amelioration of headache and contraction of MMA, but the MCA remained unchanged. Exploratory analysis revealed www.selleckchem.com/p38-MAPK.html that in attacks with unilateral headache, there was only dilation of the ipsilateral Selleckchem CP673451 and no dilation of the contralateral MMA and of the MCA. In bilateral headache, bilateral vasodilation of both MMA and MCA became apparent. These data suggest that migraine without aura is accompanied by dilation of extracerebral and intracerebral arteries and that the headache location correlates with the location of the vasodilation. Furthermore, contraction of extracerebral, and not intracerebral arteries, is associated with amelioration of headache. Taken together,

these observations support a role for vasodilation and potential perivascular release of vasoactive substances in migraine generation. Functional Correlates.— With improved neurophysiological and functional MCE公司 imaging techniques, it became evident that migraine is associated with distinct patterns of neuronal and glial activation.36 The correct interpretation of imaging data, however, relies on distinguishing the signal alterations induced by migraine from those of a general pain response. One way of achieving this is to compare areas of activation and deactivation present during the migraine attack, to signal changes occurring after effective abortive therapy.7 The areas responsible for pain are expected to change following

effective therapy. Persistence of hyperactivity in an area represents evidence in favor of its role as a migraine-triggering site (see Table 2 for a list of neuroimaging findings during migraine attack). In several studies after sumatriptan administration, for example, the dorsal pons remained activated.37-39 An important early PET study from Weiller and collaborators39 demonstrated specific changes in blood flow during migraine attacks that do not follow a neurovascular distribution and are distinct from the patterns of blood flow seen during other primary headache disorders. Increased blood flow was found during spontaneous attacks in the brainstem and in the cingulate, auditory, and visual association cortices. Only contalateral brainstem activation, however, persisted after sumatriptan injection had induced complete relief from headache and phonophobia and photophobia.

Asghar and collaborators35 examined the diameter of extracranial

Asghar and collaborators35 examined the diameter of extracranial and intracranial vessels in subjects suffering from migraine without aura, seeking to avoid a premature dismissal of vascular mechanisms. A novel high-resolution direct MRA imaging technique was used to measure arterial circumference of the extracranial

MMA and the intracranial middle cerebral artery (MCA). The study found dilation of both MMA and MCA during migraine attack. Sumatriptan administration caused amelioration of headache and contraction of MMA, but the MCA remained unchanged. Exploratory analysis revealed BIBW2992 nmr that in attacks with unilateral headache, there was only dilation of the ipsilateral Ipilimumab ic50 and no dilation of the contralateral MMA and of the MCA. In bilateral headache, bilateral vasodilation of both MMA and MCA became apparent. These data suggest that migraine without aura is accompanied by dilation of extracerebral and intracerebral arteries and that the headache location correlates with the location of the vasodilation. Furthermore, contraction of extracerebral, and not intracerebral arteries, is associated with amelioration of headache. Taken together,

these observations support a role for vasodilation and potential perivascular release of vasoactive substances in migraine generation. Functional Correlates.— With improved neurophysiological and functional 上海皓元医药股份有限公司 imaging techniques, it became evident that migraine is associated with distinct patterns of neuronal and glial activation.36 The correct interpretation of imaging data, however, relies on distinguishing the signal alterations induced by migraine from those of a general pain response. One way of achieving this is to compare areas of activation and deactivation present during the migraine attack, to signal changes occurring after effective abortive therapy.7 The areas responsible for pain are expected to change following

effective therapy. Persistence of hyperactivity in an area represents evidence in favor of its role as a migraine-triggering site (see Table 2 for a list of neuroimaging findings during migraine attack). In several studies after sumatriptan administration, for example, the dorsal pons remained activated.37-39 An important early PET study from Weiller and collaborators39 demonstrated specific changes in blood flow during migraine attacks that do not follow a neurovascular distribution and are distinct from the patterns of blood flow seen during other primary headache disorders. Increased blood flow was found during spontaneous attacks in the brainstem and in the cingulate, auditory, and visual association cortices. Only contalateral brainstem activation, however, persisted after sumatriptan injection had induced complete relief from headache and phonophobia and photophobia.

Previous studies evaluated the US findings of haemophilic joints

Previous studies evaluated the US findings of haemophilic joints [32,35] and described a systematic protocol for data acquisition of US findings in haemophilic joints [30,36]. Nevertheless, the value of this technique for the assessment of haemophilic arthropathy in comparison with MRI and physical examination has not been fully evaluated so far. As a result, this technique has been underemployed in clinical practice. Another challenge of US relates to the interpretation of images and comparison with other diagnostic tests. Further studies comparing US and MRI are needed to quantitate the diagnostic sensitivity loss of US (for central aspects

of the joint which are deeper in nature) with special regard to the interpretation of subchondral abnormalities

and cartilage loss. Haemophilic pseudotumours are chronic, NVP-LDE225 datasheet encapsulated and hemorrhagic fluid collections that contain coagulated blood and are surrounded by a thick wall. They usually destroy adjacent bone and may become quite large. Both MRI and contrast-enhanced computed tomography (CT) are useful in determining the thickness of the wall and the extent of the lesion [4,37]. In the acute stage, the centre of the pseudotumour appears hypodense on CT, but the periphery is isodense and indistinguishable www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html from surrounding muscle [32]. CT shows the thick wall of pseudotumours more consistently than US does. Multiple irregular echoes on US may represent solid material that cannot be documented on CT. Differential diagnosis from abscesses may be difficult. Radiosynoviorthesis MCE is effective in limiting the frequency of joint haemorrhage, decreasing pain and improving the

function in haemophiliacs [38]. Blood-pool indices can be used to evaluate the efficacy of radioisotopic synoviorthesis (90Y and 186Re radiosynovectomy) in patients with haemophilic synovitis, and therefore can be an objective means for monitoring therapy response in these patients. An in vivo method for erythrocyte labelling with Technetium-99 m generates a dynamic perfusion sequence, which is obtained using a scintillation camera positioned over the area to be examined [39]. This demonstrates the vascularity of the tissue. Subsequently, equilibrium blood-pool images of the area are obtained and analysed with a densitometer to assess relative regional blood volume. In patients who are not bleeding but have chronic arthropathy, vascularity is not increased, and the blood volume of comparable joints may be similar. By contrast, marked increases in vascularity and image density are typically observed in studies of acute bleeding joints. Chronic hemarthroses are typically associated with persistent, but less marked increases in joint perfusion. Transient increases in joint vascularity are demonstrated after insertion of prostheses. In a patient with a thigh haematoma, the dimensions of the haemorrhage can be clearly delineated.

In vitro experiments using gastric tumor cell lines, murine model

In vitro experiments using gastric tumor cell lines, murine models and one clinical study provided evidence for a potential role of PAR2 in Helicobacter pylori-induced gastritis. Aim:  To investigate PAR2 expression in H. pylori-infected patients and correlation with proinflammatory IL-8, IL-1β as well as histologic changes of the mucosa. Furthermore, PAR2 expression was studied in context to mucosal selleck screening library amounts of secretory leukocyte protease inhibitor (SLPI), a putative

regulator of PAR2. Methods:  Twenty-two H. pylori-infected patients and 72 H. pylori-negative subjects underwent upper GI endoscopy. In antrum-derived mucosal biopsies, PAR2, IL-1β, Sirolimus mw IL-8, and SLPI expression was analyzed by quantitative RT-PCR, and in part by ELISA and immunohistochemistry. Histopathologic evaluation of gastritis was performed according to the updated Sydney classification. Results: IL-8 gene expression was 5-fold increased in the mucosa of H. pylori-infected patients compared with

non-infected (p < .0001), whereas no differences for PAR2 and IL-1β mRNA amounts were observed between both groups. PAR2 gene expression correlated positively with transcript levels of IL-8, IL-1β as well mucosal SLPI levels in H. pylori-infected patients (r: 0.47–0.84; p < .0001), whereas no correlation was found with the degree of gastritis. Conclusions:  PAR2 represents an additive pathway of IL-8 secretion and proinflammatory effects in H. pylori-induced gastritis. Reduced SLPI

levels leading to higher serine protease activities in the mucosa of infected subjects might regulate PAR2 activation. “
“Background:  High-molecular-weight cell-associated proteins (HM-CAP) assay is the most popular serological immunoassay worldwide and has been developed from US isolates as the antigens. The accuracy is reduced when the sera are from adults and children in East Asia including MCE Japan. To overcome the reduced accuracy, an enzyme immunoassay using Japanese strain–derived HM-CAP (JHM-CAP) was developed, in which the antigens were prepared by exactly the same procedure as HM-CAP. The performance of JHM-CAP was better than that of HM-CAP in Japanese adults as well as in children. The higher sensitivity was because of the presence of 100-kDa protein that was absent in the preparation of HM-CAP antigen. Materials and Methods:  Immunoblot analysis and peptide mass fingerprinting methods were used to identify the distinctive 100-kDa protein present in JHM-CAP antigens. The peptide sequence and identification were analyzed by Mascot Search on the database of Helicobacter pylori. The identified protein was confirmed by immunoblot with a specific antibody and inhibition assay by the sera.

This opened up the possibility of having a unique marker for the

This opened up the possibility of having a unique marker for the defective allele in every family segregating haemophilia A. At first, with the expensive and laborious sequencing methods available, it was

necessary to screen using techniques that could show altered behaviour in a small fragment, which was then sequenced [17]. The advent of first generation sequencing machines made it feasible to sequence an entire coding region without a screening step. It meant that we could find a mutation in one-to-two weeks. As a result of this sequencing, Selleckchem CDK inhibitor it soon became evident that there was no plausible disease-causing mutation in about half the severely affected cases. Jane Gitschier returned to the F8 gene to show that, in such cases, there was an inversion involving either

of two copies of an intronic gene F8A located within intron 22 and an extragenic copy of F8A located 400 kb upstream [18]. The international haemophilia A database, which I started in 1991 [19] to improve understanding of the correlation check details between mutation and phenotype, went online in 1996 [20]. From a critical analysis of the mutations published up to that date, we discovered that some mutations had a highly variable phenotype and that there was a stronger risk of inhibitor development for some types of mutation than others [21]. The database has grown steadily and as of 2004 listed over 1000 unique mutations. This is set to increase massively with the next update and overhaul of the site in 2012. The most recent technical advance in detection of foetal DNA in maternal blood now allows the status of a foetus to be determined as early as week 11 of gestation [22]. In the next 50 years, genetic tools will come to dominate not only diagnosis but treatment of the haemophilias, which after all are the classic

example of genetic disorder in man. Many recent enhancements to processes medchemexpress used in genetic analysis of inherited bleeding disorders are available. They are reviewed here following the pathway from patient referral to reporting of results. Computer-based laboratory information management systems (LIMS) can provide a complete system of ‘paperless’ sample management. All patient referral documentation can be scanned and stored electronically, work lists can be generated for testing to be undertaken, and results can subsequently be recorded within the LIMS. Genomic DNA can be prepared from blood and other tissues using a variety of automated extraction procedures. Bar-coding of individual samples and of the plates in which they are analysed facilitates recording storage location and ensures that the correct samples are transferred between containers during analysis. Several genetic analysis techniques are available, generally utilizing genomic DNA as template.

This opened up the possibility of having a unique marker for the

This opened up the possibility of having a unique marker for the defective allele in every family segregating haemophilia A. At first, with the expensive and laborious sequencing methods available, it was

necessary to screen using techniques that could show altered behaviour in a small fragment, which was then sequenced [17]. The advent of first generation sequencing machines made it feasible to sequence an entire coding region without a screening step. It meant that we could find a mutation in one-to-two weeks. As a result of this sequencing, DNA Damage inhibitor it soon became evident that there was no plausible disease-causing mutation in about half the severely affected cases. Jane Gitschier returned to the F8 gene to show that, in such cases, there was an inversion involving either

of two copies of an intronic gene F8A located within intron 22 and an extragenic copy of F8A located 400 kb upstream [18]. The international haemophilia A database, which I started in 1991 [19] to improve understanding of the correlation this website between mutation and phenotype, went online in 1996 [20]. From a critical analysis of the mutations published up to that date, we discovered that some mutations had a highly variable phenotype and that there was a stronger risk of inhibitor development for some types of mutation than others [21]. The database has grown steadily and as of 2004 listed over 1000 unique mutations. This is set to increase massively with the next update and overhaul of the site in 2012. The most recent technical advance in detection of foetal DNA in maternal blood now allows the status of a foetus to be determined as early as week 11 of gestation [22]. In the next 50 years, genetic tools will come to dominate not only diagnosis but treatment of the haemophilias, which after all are the classic

example of genetic disorder in man. Many recent enhancements to processes 上海皓元 used in genetic analysis of inherited bleeding disorders are available. They are reviewed here following the pathway from patient referral to reporting of results. Computer-based laboratory information management systems (LIMS) can provide a complete system of ‘paperless’ sample management. All patient referral documentation can be scanned and stored electronically, work lists can be generated for testing to be undertaken, and results can subsequently be recorded within the LIMS. Genomic DNA can be prepared from blood and other tissues using a variety of automated extraction procedures. Bar-coding of individual samples and of the plates in which they are analysed facilitates recording storage location and ensures that the correct samples are transferred between containers during analysis. Several genetic analysis techniques are available, generally utilizing genomic DNA as template.

This opened up the possibility of having a unique marker for the

This opened up the possibility of having a unique marker for the defective allele in every family segregating haemophilia A. At first, with the expensive and laborious sequencing methods available, it was

necessary to screen using techniques that could show altered behaviour in a small fragment, which was then sequenced [17]. The advent of first generation sequencing machines made it feasible to sequence an entire coding region without a screening step. It meant that we could find a mutation in one-to-two weeks. As a result of this sequencing, http://www.selleckchem.com/products/MK-2206.html it soon became evident that there was no plausible disease-causing mutation in about half the severely affected cases. Jane Gitschier returned to the F8 gene to show that, in such cases, there was an inversion involving either

of two copies of an intronic gene F8A located within intron 22 and an extragenic copy of F8A located 400 kb upstream [18]. The international haemophilia A database, which I started in 1991 [19] to improve understanding of the correlation GS-1101 mouse between mutation and phenotype, went online in 1996 [20]. From a critical analysis of the mutations published up to that date, we discovered that some mutations had a highly variable phenotype and that there was a stronger risk of inhibitor development for some types of mutation than others [21]. The database has grown steadily and as of 2004 listed over 1000 unique mutations. This is set to increase massively with the next update and overhaul of the site in 2012. The most recent technical advance in detection of foetal DNA in maternal blood now allows the status of a foetus to be determined as early as week 11 of gestation [22]. In the next 50 years, genetic tools will come to dominate not only diagnosis but treatment of the haemophilias, which after all are the classic

example of genetic disorder in man. Many recent enhancements to processes MCE公司 used in genetic analysis of inherited bleeding disorders are available. They are reviewed here following the pathway from patient referral to reporting of results. Computer-based laboratory information management systems (LIMS) can provide a complete system of ‘paperless’ sample management. All patient referral documentation can be scanned and stored electronically, work lists can be generated for testing to be undertaken, and results can subsequently be recorded within the LIMS. Genomic DNA can be prepared from blood and other tissues using a variety of automated extraction procedures. Bar-coding of individual samples and of the plates in which they are analysed facilitates recording storage location and ensures that the correct samples are transferred between containers during analysis. Several genetic analysis techniques are available, generally utilizing genomic DNA as template.

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonis

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonist analgesic properties. Its most frequent side effect is sedation. Nalbuphine can produce respiratory depression but is considered to have low abuse potential.2 Tramadol hydrogen chloride is an “atypical” opioid used for pain management.3 Tramadol weakly binds the mu opioid receptor and

also inhibits serotonin and PD0325901 clinical trial norepinephrine re-uptake. Tramadol is better tolerated than other opioids because of its low impact on the respiratory, cardiac, and gastrointestinal (GI) systems at therapeutic doses. There is evidence that all opioids can sensitize the central nervous system to pain (especially in migraineurs) and increase the risk of medication-overuse headache.4 Klapper and Stanton compared meperidine 75 mg plus hydroxyzine 75 mg intramuscular (IM) with DHE 1 mg plus metoclopramide 10 mg to treat patients whose abortives had failed.5 Pain reduction measured on a 4-point pain scale (PPS) (4-PPS) was greater with DHE/metoclopramide (−2.14 vs −0.86, P = .006), as was the percentage with headache relief (93% vs 21%, P < .001). Carleton et al compared meperidine 1.5 mg/kg plus hydroxyzine 0.7 mg/kg IM with DHE 1 mg plus hydroxyzine 0.7 mg/kg IM.6 There was similar efficacy in pain reduction measured on a visual analog scale (VAS) (55.7% vs 53.5%, P = .81). Dizziness (DHE 2% vs meperidine 15%,

P < .05) and drowsiness (DHE 21.5% vs meperidine 22.6%) were the most common side effects. Davis et al compared meperidine 75 mg plus promethazine 25 mg IM with ketorolac 60 mg IM, and rates of headache relief at 1 hour were not significantly different (63.3% vs 50%, respectively; P = .37).7 Duarte Tipifarnib et al found that headache relief was similar between meperidine 100 mg plus hydroxyzine 50 mg IM and ketorolac 60 mg IM.8 Harden et al also found pain reduction (VAS) to be similar between meperidine 50 mg plus promethazine 25 mg IM, ketorolac 60 mg IM, and placebo/ normal saline (NS) IM (60% vs 44.4% vs 54.5%).9 Lane et al compared

meperidine 0.4 mg/kg plus dimenhydrinate 25 mg intravenous (IV) with chlorpromazine 0.1 mg/kg IV (up to 3 doses); pain reduction (VAS) was significantly greater 上海皓元医药股份有限公司 with prochlorperazine (−70.6 vs −44.5, P < .05).10 Larkin and Prescott compared meperidine 75 mg IM with ketorolac 30 mg IM, and headache relief at 1 hour was greater with meperidine (44% vs 13%, P < .02).11 Richman et al compared meperidine 1.5 mg/kg IM with droperidol 2.5 mg; there was no difference in pain reduction (VAS) (−37 vs −47, P = .33).12 Belgrade et al compared meperidine 75 mg IM plus hydroxyzine 50 mg IM with DHE 1 mg plus metoclopramide 10 mg IV and to butorphanol 2 mg IM.13 Pain reduction (VAS) was greater with DHE plus metoclopramide (−59) and butorphanol (−54) vs meperidine/hydroxyzine (−37, P < .01). Patients experienced greater than 90% pain reduction more often in the DHE/metoclopramide group (38%) vs butorphanol (16%) or meperidine/hydroxyzine (0%, P < .01).

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonis

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonist analgesic properties. Its most frequent side effect is sedation. Nalbuphine can produce respiratory depression but is considered to have low abuse potential.2 Tramadol hydrogen chloride is an “atypical” opioid used for pain management.3 Tramadol weakly binds the mu opioid receptor and

also inhibits serotonin and DZNeP mouse norepinephrine re-uptake. Tramadol is better tolerated than other opioids because of its low impact on the respiratory, cardiac, and gastrointestinal (GI) systems at therapeutic doses. There is evidence that all opioids can sensitize the central nervous system to pain (especially in migraineurs) and increase the risk of medication-overuse headache.4 Klapper and Stanton compared meperidine 75 mg plus hydroxyzine 75 mg intramuscular (IM) with DHE 1 mg plus metoclopramide 10 mg to treat patients whose abortives had failed.5 Pain reduction measured on a 4-point pain scale (PPS) (4-PPS) was greater with DHE/metoclopramide (−2.14 vs −0.86, P = .006), as was the percentage with headache relief (93% vs 21%, P < .001). Carleton et al compared meperidine 1.5 mg/kg plus hydroxyzine 0.7 mg/kg IM with DHE 1 mg plus hydroxyzine 0.7 mg/kg IM.6 There was similar efficacy in pain reduction measured on a visual analog scale (VAS) (55.7% vs 53.5%, P = .81). Dizziness (DHE 2% vs meperidine 15%,

P < .05) and drowsiness (DHE 21.5% vs meperidine 22.6%) were the most common side effects. Davis et al compared meperidine 75 mg plus promethazine 25 mg IM with ketorolac 60 mg IM, and rates of headache relief at 1 hour were not significantly different (63.3% vs 50%, respectively; P = .37).7 Duarte Selleck Ku-0059436 et al found that headache relief was similar between meperidine 100 mg plus hydroxyzine 50 mg IM and ketorolac 60 mg IM.8 Harden et al also found pain reduction (VAS) to be similar between meperidine 50 mg plus promethazine 25 mg IM, ketorolac 60 mg IM, and placebo/ normal saline (NS) IM (60% vs 44.4% vs 54.5%).9 Lane et al compared

meperidine 0.4 mg/kg plus dimenhydrinate 25 mg intravenous (IV) with chlorpromazine 0.1 mg/kg IV (up to 3 doses); pain reduction (VAS) was significantly greater medchemexpress with prochlorperazine (−70.6 vs −44.5, P < .05).10 Larkin and Prescott compared meperidine 75 mg IM with ketorolac 30 mg IM, and headache relief at 1 hour was greater with meperidine (44% vs 13%, P < .02).11 Richman et al compared meperidine 1.5 mg/kg IM with droperidol 2.5 mg; there was no difference in pain reduction (VAS) (−37 vs −47, P = .33).12 Belgrade et al compared meperidine 75 mg IM plus hydroxyzine 50 mg IM with DHE 1 mg plus metoclopramide 10 mg IV and to butorphanol 2 mg IM.13 Pain reduction (VAS) was greater with DHE plus metoclopramide (−59) and butorphanol (−54) vs meperidine/hydroxyzine (−37, P < .01). Patients experienced greater than 90% pain reduction more often in the DHE/metoclopramide group (38%) vs butorphanol (16%) or meperidine/hydroxyzine (0%, P < .01).

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonis

Nalbuphine is a semisynthetic opioid with mixed agonist–antagonist analgesic properties. Its most frequent side effect is sedation. Nalbuphine can produce respiratory depression but is considered to have low abuse potential.2 Tramadol hydrogen chloride is an “atypical” opioid used for pain management.3 Tramadol weakly binds the mu opioid receptor and

also inhibits serotonin and Tyrosine Kinase Inhibitor Library cost norepinephrine re-uptake. Tramadol is better tolerated than other opioids because of its low impact on the respiratory, cardiac, and gastrointestinal (GI) systems at therapeutic doses. There is evidence that all opioids can sensitize the central nervous system to pain (especially in migraineurs) and increase the risk of medication-overuse headache.4 Klapper and Stanton compared meperidine 75 mg plus hydroxyzine 75 mg intramuscular (IM) with DHE 1 mg plus metoclopramide 10 mg to treat patients whose abortives had failed.5 Pain reduction measured on a 4-point pain scale (PPS) (4-PPS) was greater with DHE/metoclopramide (−2.14 vs −0.86, P = .006), as was the percentage with headache relief (93% vs 21%, P < .001). Carleton et al compared meperidine 1.5 mg/kg plus hydroxyzine 0.7 mg/kg IM with DHE 1 mg plus hydroxyzine 0.7 mg/kg IM.6 There was similar efficacy in pain reduction measured on a visual analog scale (VAS) (55.7% vs 53.5%, P = .81). Dizziness (DHE 2% vs meperidine 15%,

P < .05) and drowsiness (DHE 21.5% vs meperidine 22.6%) were the most common side effects. Davis et al compared meperidine 75 mg plus promethazine 25 mg IM with ketorolac 60 mg IM, and rates of headache relief at 1 hour were not significantly different (63.3% vs 50%, respectively; P = .37).7 Duarte buy ABT-263 et al found that headache relief was similar between meperidine 100 mg plus hydroxyzine 50 mg IM and ketorolac 60 mg IM.8 Harden et al also found pain reduction (VAS) to be similar between meperidine 50 mg plus promethazine 25 mg IM, ketorolac 60 mg IM, and placebo/ normal saline (NS) IM (60% vs 44.4% vs 54.5%).9 Lane et al compared

meperidine 0.4 mg/kg plus dimenhydrinate 25 mg intravenous (IV) with chlorpromazine 0.1 mg/kg IV (up to 3 doses); pain reduction (VAS) was significantly greater 上海皓元 with prochlorperazine (−70.6 vs −44.5, P < .05).10 Larkin and Prescott compared meperidine 75 mg IM with ketorolac 30 mg IM, and headache relief at 1 hour was greater with meperidine (44% vs 13%, P < .02).11 Richman et al compared meperidine 1.5 mg/kg IM with droperidol 2.5 mg; there was no difference in pain reduction (VAS) (−37 vs −47, P = .33).12 Belgrade et al compared meperidine 75 mg IM plus hydroxyzine 50 mg IM with DHE 1 mg plus metoclopramide 10 mg IV and to butorphanol 2 mg IM.13 Pain reduction (VAS) was greater with DHE plus metoclopramide (−59) and butorphanol (−54) vs meperidine/hydroxyzine (−37, P < .01). Patients experienced greater than 90% pain reduction more often in the DHE/metoclopramide group (38%) vs butorphanol (16%) or meperidine/hydroxyzine (0%, P < .01).