Diameter Of Superficial Temporal Artery Research Articles

The pharmacological effect of BGC20-1531, a novel prostanoid EP4 receptor antagonist, in the Prostaglandin E2 human model of headache

Using a human Prostaglandin E2 (PGE2) model of headache, we examined whether a novel potent and selective EP4 receptor antagonist, BGC20-1531, may prevent headache and dilatation of the middle cerebral (MCA) and superficial temporal artery (STA). In a three-way cross-over trial, eight healthy volunteers were randomly allocated to receive 200 and 400 mg BGC20-1531 and placebo, followed by a 25-min infusion of PGE2. We recorded headache intensity on a verbal rating scale, MCA blood flow velocity and STA diameter. There was no difference in headache response or prevention of the dilation of the MCA or the STA (P > 0.05) with either dose of BGC20-1531 relative to placebo, although putative therapeutic exposures were not reached in all volunteers. In conclusion, these data suggest that the other EP receptors may be involved in PGE2 induced headache and dilatation in normal subjects.

Clinical and Angiographic Outcomes From Indirect Revascularization Surgery for Moyamoya Disease in Adults and Children: A Review of 63 Procedures

Several forms of indirect cerebral revascularization have been proposed to promote neovascularity to the ischemic brain. To present clinical and angiographic outcomes of indirect revascularization by encephaloduroarteriosynangiosis and burr holes for the treatment of Moyamoya disease in adults and children. Data from 63 hemispheres treated in 42 patients (average age, 30 years; 33 adults; 30 female patients; median follow-up, 14 months) were reviewed. In hemispheres with preoperative and postoperative (6- to 12-month) angiograms available, superficial temporal artery (STA) and middle meningeal artery (MMA) diameters were measured. Preoperative and postoperative corrected arterial sizes were compared. Seven patients (17%) had transient ischemic attacks that resolved within 1 month of surgery. No patients suffered moyamoya-related hemorrhage after treatment. Two patients developed additional symptoms many years after surgery. In 18 hemispheres with preoperative and postoperative angiograms, there was an average postoperative increase in STA and MMA diameters of 51% (P = .003) and 49% (P = .002), respectively. Both children and adults displayed revascularization. Two patients did not demonstrate increased vessel size. STA blush and new branches and MMA blush and new branches were identified in 12, 14, 14, and 16 hemispheres, respectively. Angiographic blush was identified in 59% of frontal and 19% of parietal burr holes (P = .03). Surgical complications included 2 subdural hemorrhages requiring evacuation and 2 new ischemic deficits (1 transient). Indirect revascularization by encephaloduroarteriosynangiosis and burr holes for moyamoya results in long-term resolution of ischemic and hemorrhagic manifestations in 95% of adults and children. The MMA appears to contribute significantly to the revascularization on follow-up angiograms with increased size and neovascularity comparable to that of the STA. Angiographically, parietal burr holes do not contribute as significantly as frontal burr holes.

Anatomic Bases of Superficial Temporal Artery and Temporal Branch of Facial Nerve

The superficial temporal artery (STA)-based flaps have been used for different reconstructive purposes. These operations may cause facial nerve injury. The variations of the STA and its relation to temporal branch of the facial nerve (TBFN) were evaluated in this study. Thirteen cadavers with 26 STA and TBFN have been dissected. The bifurcation of STA was found to be 60% above the superior border of the zygomatic arc and 40% below this level. The mean lengths of frontal and temporal branches (FB and TB) of STA were 11.5 and 11.4 cm, respectively. The mean numbers of perforators of FB and TB to deep plane were 1.30 and 1.34, respectively. The mean diameter of STA at the superior border of zygomatic arc was 2.5 mm. The mean diameters of TB and FB at the level of bifurcation were 1.8 mm and 2.0 mm, respectively. The mean number of TBFN at the level of zygomatic arc was 3.70. The mean distance of the first and last branching of TBFN to tragus was found to be 24 mm. The mean number of TBFN at the level of the middle orbita was found to be 2.7. The mean distance of first and last branches of TBFN to the lateral orbital rim was 12 and 24 mm, respectively. The results found in this study may increase the accuracy of flaps based on STA and decrease the risk of facial nerve paralysis during these operations.

Discrepancy between strong cephalic arterial dilatation and mild headache caused by prostaglandin D2 (PGD2)

Prostaglandins (PGs) are involved in nociception and mast cell degranulation. Prostaglandin D₂ (PGD₂) is a vasodilatator released during mast cell degranulation. The headache-eliciting effect of PGD₂ has not been studied in man. Twelve healthy volunteers were randomly allocated to receive intravenous infusion of 384 ng/kg/min PGD₂ over 25 min in a placebo-controlled, double-blind cross-over study. We recorded headache intensity and associated symptoms, velocity in the middle cerebral artery (V(MCA)) and diameter of the superficial temporal artery (STA) and radial artery (RA) using ultrasonography. In the period 0-14 h, 11 subjects reported headache on PGD₂ compared to one subject on placebo (P = 0.002). During the in-hospital phase (0-120 min), the area under the headache curve was larger on PGD₂ compared to placebo (P < 0.05). Median peak headache, 1 (0-1), occurred 10 min after start of PGD(2) infusion. There was no difference in incidence of headache in the post-hospital phase between PGD₂ (n = 3) and placebo (n = 1). There was a decrease in V(MCA) (P < 0.001), increase in STA (P < 0.001) and RA (P < 0.006) diameter during PGD₂ infusion compared to placebo. Peak decrease in V(MCA) was 28.3% after 10 min and peak increase in STA was 55.7% after 20 min on the PGD₂ day. The present study shows that PGD₂ is a very strong vasodilator of MCA, STA and RA, but causes only mild headache.

Prostaglandin I2 (epoprostenol) triggers migraine-like attacks in migraineurs

Prostacyclin [prostaglandin I(2) (PGI(2))] activates and sensitizes meningeal sensory afferents. In healthy subjects PGI(2) triggers headache in healthy subjects. However, the migraine-eliciting effect of PGI(2) has not been systematically studied in patients with migraine. We hypothesized that intravenous infusion of the stable prostacyclin analogue epoprostenol would trigger migraine-like attacks in migraineurs. We infused 10 ng kg(-1) min(-1) PGI(2) or placebo over 25 min in 12 migraineurs without aura in a controlled, double-blind, cross-over study and recorded headache intensity and associated symptoms, velocity in the middle cerebral artery (V(MCA)) and diameter in the superficial temporal artery. In the period 0-14 h, 12 subjects reported headache on PGI(2) day compared with three subjects on placebo day (P = 0.004), and six subjects fulfilled the criteria for an experimentally induced migraine-like attack compared with two subjects on placebo (P = 0.219). During infusion and post-infusion phases the AUC under the headache curve on PGI(2) was significantly larger than on placebo (P < 0.05). There was a significant V(MCA) decrease (P = 0.015) and superficial temporal artery diameter increase (P < 0.001) on PGI(2) compared with placebo. In conclusion, PGI(2) may trigger a migraine-like attack in migraine sufferers. We suggest sensitization of perivascular nociceptors and arterial dilation as the mode of action of PGI(2)-induced headache and migraine-like attacks.

Postoperative Evaluation of Changes in Extracranial-Intracranial Bypass Graft Using Superficial Temporal Artery Duplex Ultrasonography

Extracranial-intracranial (ECIC) bypass grafts have been assessed postoperatively by various neuroradiologic techniques. The aim of this prospective study was to evaluate postoperative changes in ECIC bypass graft by using superficial temporal artery duplex ultrasonography (STDU). Furthermore, this study assessed the ability of STDU to predict cerebrovascular reserve capacity (CVR). Forty-five consecutive patients who underwent ECIC bypass procedure for atherosclerotic internal carotid artery occlusion were enrolled in this prospective study. All patients underwent single-photon emission CT and STDU preoperatively, 14 days after, 3 months after, 1 year after, and 2 years after ECIC bypass. The diameter and flow velocities of the ipsilateral superficial temporal artery (STA), and regional cerebral blood flow (rCBF) showed increase during the first 2 weeks and then remained stable, whereas CVR showed a constant improvement up to 2 years after surgery. The STA diameter and mean STA flow velocity correlated significantly with CVR at 1 year after surgery (r2 = 0.1232 and r2 = 0.08716, respectively; P < .05). A cutoff value of 1.8 mm STA diameter was determined as the most reliable value to predict CVR greater than 10% at 1 year after surgery. The positive predictive value was calculated as 96.6%, the negative predictive value as 43.8%, the sensitivity as 75.7%, the specificity as 87.5%, and the likelihood ratio as 6.056. ECIC bypass grafts can be assessed postoperatively in a noninvasive fashion with STDU. This technique provides information regarding patency as well as quantitative assessment of bypass function. Moreover, STDU is useful to predict CVR improvement.

The Cholinomimetic Agent Carbachol Induces Headache in Healthy Subjects

The parasympathetic nervous system is likely to be involved in migraine pathogenesis. We hypothesized that the cholinomimetic agonist carbachol would induce headache and vasodilation of cephalic and radial arteries. Carbachol (3 microg/kg) or placebo was randomly infused into 12 healthy subjects in a double-blind crossover study. Headache was scored on a verbal rating scale from 0-10. Velocity in the middle cerebral artery (V(MCA)) and diameter of the superficial temporal artery (STA) and radial artery (RA) were recorded. Nine participants developed headache after carbachol compared with three after placebo. The area under the curve for headache was increased after carbachol compared with placebo both during infusion (0-30 min) (P = 0.042) and in the postinfusion period (30-90 min) (P = 0.027). Carbachol infusion caused a drop in V(MCA) (P = 0.003) and an increase in STA diameter (P = 0.006), but no increase in the RA diameter (P = 0.200). In conclusion, the study demonstrated that carbachol caused headache and dilation of cephalic arteries in healthy subjects.

PACAP38 induces migraine-like attacks in patients with migraine without aura

Experimental studies have shown that infusion of vasoactive neurotransmitters may trigger headache or migraine-like attacks in man. Pituitary adenylate cyclase activating peptide-38 (PACAP38) is a strong vasodilator found in trigeminal sensory and parasympathetic perivascular nerve fibers. We therefore hypothesized that infusion of PACAP38 would cause headache in healthy subjects and migraine-like attacks in migraine patients. Twelve healthy subjects and 12 migraine patients were examined in two separate studies. All subjects were allocated to receive 10 pmol/kg/min PACAP38 and placebo in a randomized, double-blind crossover study design. Headache was scored on a verbal rating scale (VRS) during hospital (0-2 h) and post-hospital (2-12 h) phases. Mean blood flow velocity in the middle cerebral artery (V(MCA)) by transcranial Doppler (TCD) and diameter of the superficial temporal artery (STA) by high resolution ultrasonography were recorded during hospital phase in migraineurs. PACAP38 infusion caused headache in all healthy subjects and 11 out of 12 migraine patients. Seven migraine patients experienced migraine-like attacks after PACAP38 and none after placebo (P = 0.016). Most of attacks (6 out of 7) occurred during the post-hospital phase [mean time 6 h (range 2-11)]. Two healthy subjects reported migraine-like attacks after PACAP38 during the hospital phase and none during the post-hospital phase. In the hospital phase, the area under the curve (AUC) for headache score was larger during PACAP38 infusion compared to placebo in healthy subjects (P = 0.005) and tended to be larger in migraineurs (P = 0.066). In the post-hospital phase, the AUC for headache was larger after PACAP38 infusion compared to placebo in both healthy subjects (P = 0.005) and migraine patients (P = 0.013). In migraine patients, PACAP38 caused a peak decrease of 16.1% in V(MCA) and a 37.5% increase in STA diameter at 20 min after start of infusion. In conclusion, PACAP38 infusion caused headache and vasodilatation in both healthy subjects and migraine patients. In migraine sufferers, PACAP38 caused delayed migraine-like attacks. The findings stimulate further investigation of the neuronal and vascular mechanisms of PACAP38.

Vasoactive Intestinal Peptide Causes Marked Cephalic Vasodilation, but does not Induce Migraine

We hypothesized that intravenous infusion of the parasympathetic transmitter, vasoactive intestinal peptide (VIP), might induce migraine attacks in migraineurs. Twelve patients with migraine without aura were allocated to receive 8 pmol kg(-1) min(-1) VIP or placebo in a randomized, double-blind crossover study. Headache was scored on a verbal rating scale (VRS), mean blood flow velocity in the middle cerebral artery (V(mean MCA)) was measured by transcranial Doppler ultrasonography, and diameter of the superficial temporal artery (STA) by high-frequency ultrasound. None of the subjects reported a migraine attack after VIP infusion. VIP induced a mild immediate headache (maximum 2 on VRS) compared with placebo (P = 0.005). Three patients reported delayed headache (3-11 h after infusion) after VIP and two after placebo (P = 0.89). V(mean MCA) decreased (16.3 +/- 5.9%) and diameter of STA increased significantly after VIP (45.9 +/- 13.9%). VIP mediates a marked dilation of cranial arteries, but does not trigger migraine attacks in migraineurs. These data provide further evidence against a purely vascular origin of migraine.

The Effect of Propranolol on Glyceryltrinitrate-Induced Headache and Arterial Response

Prophylactic drug trials in migraine are long-lasting and expensive and require long-term toxicology information. A human migraine model would therefore be helpful in testing new drugs. Immediate headache and delayed migraine after glyceryltrinitrate (GTN) has been well characterized. We have recently shown that sodium valproate has prophylactic effect in the GTN model. Here we report our experience with propranolol in this model. Nineteen subjects with migraine without aura and 16 sex- and aged-matched healthy subjects were included in a two-centre randomized double-blind cross-over study. Fourteen migraine subjects and 14 healthy subjects completed the study and results from comparison of the 28 subjects are reported. Randomly propranolol 160 mg or placebo were each given daily for 14 days to both migraine and healthy subjects. A 20-min intravenous infusion of GTN 0.25 microg/kg per min was administered on a study day at the end of both pretreatment periods. Headache was registered for 12 h after GTN infusions. Its intensity was scored on a numerical verbal rating scale from 0 to 10. Fulfilment of International Headache Society (HIS) criteria was recorded for 24 h. Radial and superficial temporal artery diameters and blood velocity of both middle cerebral arteries were measured. All migraine subjects developed headache after GTN. No reduction of overall peak headache was found after propranolol (median 5, range 0-7) compared with placebo (median 5, range 0-10) (P = 0.441). Eight of the 14 completing migraine subject developed IHS 1.1 migraine after GTN, two subjects on both days, three subjects only after placebo, and three subjects only after propranolol. No reduction of GTN-induced migraine was found after propranolol compared with placebo (5 vs. 5, P = 1.000). All healthy subjects developed headache after GTN. No reduction of overall peak headache was found after propranolol (median 2, range 1-5) compared with placebo (median 1, range 1-7) (P = 0.315). Two subjects fulfilled IHS criteria 1.1 for migraine without aura after propranolol but not after placebo. The fulfilment was short lasting and did not require rescue medication. Headache after GTN was more pronounced in migraine subjects than in healthy subjects both with (P = 0.003) and without pretreatment with propranolol (P = 0.017). We found that 2 weeks of propranolol constricted the radial artery in healthy subjects but not in migraine subjects. GTN-induced vasodilatation abolished this difference. Mean maximum blood flow velocity in the middle cerebral artery was higher in healthy subjects than in migraine patients (P = 0.003-0.033) and unaffected by propranolol. We observed no effect of propranolol on GTN-induced headache and migraine. This could indicate that GTN induces migraine at a deeper level of the pathophysiological cascade of migraine than the prophylactic effect of propranolol. Propranolol does not constrict cerebral arteries, which therefore cannot be part of its mechanism of action in migraine.

The Phosphodiesterase 3 Inhibitor Cilostazol Dilates Large Cerebral Arteries in Humans without Affecting Regional Cerebral Blood Flow

Cilostazol, an inhibitor of phosphodiesterase (PDE) type 3, is used clinically in peripheral artery disease. PDE3 inhibitors may be clinically useful in the treatment of delayed cerebral vasospasm after subarachnoid hemorrhage. The authors present the first results on the effect of cilostazol on cerebral hemodynamics in normal participants. In this double-blind, randomized, crossover study, 200 mg cilostazol or placebo was administered orally to 12 healthy participants. Cerebral blood flow was measured using 133Xe inhalation and single photon emission computerized tomography. Mean flow velocity in the middle cerebral arteries (VMCA) was measured with transcranial Doppler, and the superficial temporal and radial arteries diameters were measured with ultrasonography. During the 4-hour observation period, there was no effect on systolic blood pressure (P = 0.28), but diastolic blood pressure decreased slightly compared with placebo (P = 0.04). VMCA decreased 21.5 +/- 5.7% after cilostazol and 5.5 +/- 12.2% after placebo (P = 0.02, vs. placebo), without any change in global or regional cerebral blood flow. The superficial temporal artery diameter increased 17.6 +/- 12.3% (P < 0.001 vs. baseline) and radial artery diameter increased 12.6 +/- 8.6% (P < 0.001 vs. baseline). Adverse events, especially headache, were common. The findings suggest that cilostazol is an interesting candidate for future clinical trials of delayed cerebral vasospasm.