Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many reports confirm the existence of long-range correlations between fluctuations of various physiological signals in healthy subjects and demonstrate disappearance of these correlations in pathological conditions. Blood flow velocity in intracranial vessels is changeable over time and depends on complex physiological regulatory mechanisms. The character of blood flow velocity fluctuations may indicate the presence of vascular disorders associated with various diseases. The aim of our study was to establish whether fluctuations in MCA blood flow velocity are fractal in physiological conditions and if so, whether this feature is lost in migraine, as the role of vasomotoric disturbances has been already evidenced in pathophysiology of this disease. The axial flow velocity changes averaged over a cardiac beat interval were monitored continuously via two channels through the temporal windows using a DWL Multi-DopT TCD device with 2-MHz probes. The examinations were performed in supine rest in two-hour periods in two groups: of 7 patients with clinically confirmed migraine with aura during headache-free intervals (15 recordings), and in the control group of 4 young, healthy volunteers (10 recordings). The results in the form of time series were analysed using the methods of fractal statistics. Multifractality in the recordings in physiological conditions was clearly confirmed, as well as its absence in the averaged recordings in the group of migraneurs. The findings justify a supposition that the breakdown of multifractal properties of MCA blood flow time series in migraine may result from the vasomotor disturbances present even during headache-free intervals. However, possible usefulness of this method in the diagnostics of migraine requires further investigation.
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PMID:[Fractal analysis of MCA blood flow velocity fluctuations in migraine--preliminary report]. 1517 33

A 25-year-old woman (gravida 1, para 0) who had no history indicating the toxemia of pregnancy developed hypertension and severe throbbing headache after the delivery of her first child by the cesarean section. Generalized tonic-clonic seizure ensued 5 days after the delivery, after which she did not fully regain her consciousness. Her head T2-weighted and FLAIR MRIs showed areas of multiple high intensities in the basal ganglia and cerebral white matter. Her cerebral MRA revealed the segmental stenosis and irregular wall of the major vessels, in particular of the right MCA trunk. Three weeks later, these abnormalities in the neuroimages disappeared and she was free of any symptoms. The history disclosed that obstetricians had used methylergometrine maleate for uterine contraction after delivery and then sumatriptan for her throbbing headache. We speculate that these vasoconstrictive agents might have induced the postpartum cerebral angiopathy. Postpartum cerebral angiopathy may be distinct from reversible posterior leukoencephalopathy in that the abnormalities are not restricted to the posterior lobes and that the vascular changes are apparent on neuroimagings. However, this entity might have a common underlying physiology, which is the abnormally elevated blood pressure that occurs in the setting of early postpartum period. Caution should be exercised when vasoconstrictives are to be used in postpartum period.
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PMID:[Postpartum cerebral angiopathy--a case report the vasculopathy associated with co-administration of two vasoconstrictives, methylergometrine maleate and sumatriptan]. 1519 57

Cortical hypersensitivity and absent habituation to different stimuli have been observed in migraine patients. These features might also be transmitted to the cerebral vasoreactivity, but results are conflicting so far. Transcranial Doppler ultrasound (TCD) was used to assess cerebral blood flow velocity (CBFV) changes in the middle (MCA) and posterior cerebral arteries (PCA) in relation to repetitive checkerboard visual stimulation. Stimulation consisted of 10 consecutive cycles, each comprising 10 s stimulation and 10 s rest. TCD recordings were analysed using stimulus-related averaging algorithm. Data of 19 interictal migraineurs with aura were compared to those of 19 headache-free healthy volunteers. The CBFV increase in PCA and in MCA during visual stimulation was significantly larger and steeper in migraineurs than in controls (P = 0.017 and P = 0.005). The response in PCA remained stable over the 10 stimulation cycles, both in migraineurs and in controls. The response in MCA was stable only in migraineurs. In controls it decreased over the last 5 stimulation cycles compared with the first 5 cycles (P = 0.04). Migraineurs with aura exhibit a larger cerebrovascular response to repetitive visual stimulation compared to headache-free subjects. A reduced adaptation to environmental stimuli in migraine is suggested, since there was no habituation in migraineurs in contrast to healthy controls.
Cephalalgia 2004 Sep
PMID:Cerebrovascular response to repetitive visual stimulation in interictal migraine with aura. 1531 25

BIBN4096BS is a CGRP-antagonist effective in the treatment of migraine. Blocking the receptor of a strong vasodilator involves a theoretical risk of causing cerebral vasoconstriction, a probability not previously investigated with BIBN4096BS. Seven healthy volunteers completed this double-blinded placebo-controlled crossover study. The volunteers received randomly 10 min infusions of either placebo, 2.5 mg or 10 mg of BIBN4096BS on 3 separate days. Transcranial Doppler was used to measure the middle cerebral artery blood flow velocity (V(MCA)); global and regional cerebral blood flow (rCBF(MCA)) was measured by 133-Xenon inhalation SPECT. The diameter of the temporal and radial artery was measured by high-resolution ultrasound. Systemic haemodynamics and partial pressure of CO(2) (P(et)CO(2)), and adverse events were monitored regularly. BIBN4096BS had no influence on global or regional cerebral blood flow, or on the blood flow velocity in the middle cerebral artery. There was no effect on systemic haemodynamics and adverse events were minor. We conclude that there is no effect of CGRP-receptor blockade on the cerebral or systemic circulation in humans. Circulating CGRP is therefore not likely to exert a vasodilatory activity in the resting state and the use of BIBN4096BS for acute migraine seems to be without risk of cerebral vasoactivity. These data suggest that BIBN4096BS is the first specific antimigraine drug without vasoactive effect.
Cephalalgia 2005 Feb
PMID:The CGRP-antagonist, BIBN4096BS does not affect cerebral or systemic haemodynamics in healthy volunteers. 1565 51

Adenosine is an endogenous neurotransmitter that is released from the brain during hypoxia and relaxes isolated human cerebral arteries. Many cerebral artery dilators cause migraine attacks. However, the effect of intravenous adenosine on headache and cerebral artery diameter has not previously been investigated in man and reports regarding the effect of intravenous adenosine on cerebral blood flow are conflicting. Twelve healthy participants received adenosine 80, 120 microg kg(-1) min(-1) and placebo intravenously for 20 min, in a double-blind, three-way, crossover, randomized design. Headache was rated on a verbal scale (0-10). Regional cerebral blood flow (rCBF) with 133Xe inhalation and single-photon emission computed tomography (SPECT) and MCA flow velocity (V(MCA)) with transcranial Doppler, were measured in direct sequence. Six participants developed headache during 80 microg kg(-1) min(-1) and six during 120 microg kg(-1) min(-1) compared with none on placebo (P = 0.006). The headache was very mild and predominantly described as a pressing sensation. When correcting data for adenosine-induced hyperventilation, no significant changes in rCBF (P = 0.22) or V(MCA) (P = 0.16) were found between treatments. A significant dilation of the superficial temporal artery (STA) was seen (P < 0.001). These results show that circulating adenosine has no effect on rCBF or V(MCA), while it dilates the STA and causes very mild headache.
Cephalalgia 2005 May
PMID:The effect of circulating adenosine on cerebral haemodynamics and headache generation in healthy subjects. 1583 52

Nontraumatic arterial dissection of the anterior cerebral artery (NAD-ACA) is a relatively rare disease entity, although case reports have recently been increased. We treated 6 patients suffering from NAD-ACA from January 1996 to December 2003, and the neuroradiological findings together with the clinical courses were reviewed. There were 3 males and 3 females with a mean age of 57.7-year-old, ranging from 41 to 65. Five patients had a past history of hypertension and one diabetes mellitus. At the onset, all patients presented with clinical manifestations of cerebral ischemia. Among them, all exhibited contralateral hemiparesis with greater weakness of the lower extremity, and two patients exhibited headache. Initial angiography revealed the pearl and string sign in four patients and string sign, tapered occlusion in each one. Follow-up angiographies revealed sequential changes in all patients; four improved and two progressed. Main anatomic site of the lesion was as follows; five in the A2 and one in the A1 portion, in addition, one patient was complicated by saccular aneurysm, one by PCA dissection, and two had with saccular aneurysm contralateral ACA & MCA and VA dissection each other. Four patients were treated conservatively by intravenous administration of argatroban, one by intravenous administration of Dextrane and one by anti-platelet agent in the acute stage. All patients were treated by anti-platelet agents in the chronic stage. Good recovery was achieved in five patients, but one who suffered from severe subarachnoid hemorrhage in the chronic stage died. Our experience suggests that hypertension and/or the succeeding abnormal structural changes in the arterial wall may contribute to the occurrence of this disease. NAD-ACA showing clinical manifestations of cerebral ischemia could result in a relatively good prognosis; however, attention should be paid to patients treated conservatively with a very closed follow-up angiography to prevent a possibility of severe hemorrhage.
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PMID:[Nontraumatic arterial dissection of the anterior cerebral artery: six cases report]. 1602 47

A case of subarachnoid hemorrhage (SAH) resulting from a ruptured intracranial dissecting aneurysm of the internal carotid artery (ICA) is reported. A 58-year-old woman presented with headache and vomiting. A CT showed diffuse SAH. A cerebral angiography demonstrated a dissecting aneurysm at the C2 segment of the right ICA. In the present case, trapping with STA-MCA anastomosis was performed and the postoperative course was uneventful. Postoperative follow-up cerebral angiogram detected no aneurysm. SAH caused by the rupture of a dissecting aneurysm of the ICA has been considered rare. To our knowledge, there have been only 29 cases. We discuss the clinical characteristics with a review of the literature.
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PMID:[Subarachnoid hemorrhage caused by a dissecting aneurysm of the internal carotid artery: case report and review of the literature]. 1609 9

The role of the parasympathetic nervous system in the pathogenesis of migraine is disputed. The headache-eliciting effect of the parasympathetic neurotransmitter, vasoactive intestinal polypeptide (VIP), and its effect on cerebral arteries and brain haemodynamics has not been systematically studied in man. We hypothesized that infusion of VIP might induce headache in healthy subjects and cause changes in cerebral haemodynamics. VIP (8 pmol/kg per min) or placebo (0.9% saline) was infused for 25 min into 12 healthy young volunteers in a crossover, double-blind design. Headache was scored on a verbal rating scale from 0 to 10, regional cerebral blood flow (rCBF) was measured with single-photon emission computed tomography and (133)Xe inhalation and mean flow velocity in the middle cerebral artery (V(meanMCA)) was measured with transcranial Doppler ultrasonography. The headache was very mild with a maximum score of 2 and described as a pressing or throbbing sensation. Five participants developed headache during VIP and one during placebo. During the infusion, a significant drop in V(meanMCA) was seen for VIP compared with placebo (P < 0.001), but the effect quickly waned and no difference was found when comparing the time between 30 and 120 min. In addition, no significant difference in the diameter of the MCA could be found during the infusion. No significant differences in rCBF (P = 0.10) were found between VIP and placebo. A marked dilation of the superficial temporal artery was seen (P = 0.04) after VIP in the first 30 min but no difference was found when comparing the time between 30 and 120 min. We found no difference in mean arterial blood pressure between VIP and placebo days but the heart rate increased significantly on a VIP day compared with a placebo day (AUC(0-30 min), P < 0.001). Plasma VIP was significantly higher on a VIP day compared with placebo (AUC(0-80 min), P < 0.001). These results show that VIP causes a decrease in V(meanMCA) without affecting rCBF. In spite of a marked vasodilator effect in the extracranial vessels and increased plasma VIP, healthy subjects developed only a very mild headache.
Cephalalgia 2006 Aug
PMID:Vasoactive intestinal polypeptide evokes only a minimal headache in healthy volunteers. 1688 36

A 61-year-old man presented with the complaint of headache. Investigations revealed a fusiform middle cerebral artery aneurysm at the M2 part. The formation of the aneurysm rapidly developed to a partially thrombosed aneurysm in the course of four months. As regards the treatment of the aneurysm, at first we tried surgery with a superficial temporal artery middle cerebral artery bypass (STA-MCA bypass) and trapping of the aneurysm. However, during the procedure, it was difficult to control bleeding from the temporal muscle, bone flap, and subdural space. Because of this, we finished the STA-MCA bypass without trapping of the aneurysm and then, four days later, we confirmed bypass patency and treated the aneurysm using endovascular coil embolization. Based on both surgical and interventional investigations in this case and a review of the reported literature, the authors propose that there are two mechanisms causing the middle cerebral artery fusiform aneurysm to develop thrombosed formation rapidly: (i) Peripheral middle cerebral artery branches demand less blood flow than other major trunk arteries. (ii) Bypass flow maintains perfusion to the distal branches. On the other hand, this flow alteration caused by surgical vascular bypass may promote the development of the aneurysm to thrombosed formation. The treatment of a fusiform middle cerebral artery aneurysm at the M2 part is also discussed.
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PMID:[A case of spontaneous fusiform aneurysm in a middle cerebral artery branch which causes rapidly thrombosed formation in a short period]. 1804 29

Spontaneous intracranial artery dissection (SIAD), leading to occlusion or stenosis of arterial lumen is a frequent but less studied cause of ischemic stroke especially in young adults. We studied 17 patients (10 men, 7 women, mean age 27.5 +/- 8.5 years) with SIAD. All the patients have undergone magnetic resonance imaging of the head, magnetic resonance angiography (MRA) (in 16 patients--follow-up MRA), 1 patient--conventional cerebral angiography. SIAD was located in the middle cerebral artery (MCA, 14 patients); posterior cerebral artery (PCA, 2 patients) and basilar artery (BA, 1 patient). Fifteen patients (88%) with SIAD developed ischemic stroke, 2 patients (12%)--a transient ischemic attack (TIA). The appearance of the local brain ischemia symptoms was combined with headache in 93% cases. The course of ischemic stroke was favorable in most cases with complete or good functional recovery in 66% of patients. A fatal outcome was observed in 1 patient (7%) with massive brain infarct. The initial cerebral angiography carried out in most cases (76%) within 3 weeks after the disease onset revealed occlusion (71%) or stenosis (29%) of corresponding cerebral arteries (MCA, PCA, BA). The last cerebral angiography conducted in 90% cases 4,5 months or later showed positive dynamics--appearance or improvement of the blood flow in these arteries--in 82% patients. The factors provoking SIAD were alcohol, contraceptive drugs and less frequent recent infection. None of patients had atherosclerosis, vasculitis or arterial hypertension. Clinical manifestations of connective tissue weakness were in 71% of patients, hypotension--65%, mitral valve prolapse--46%. In conclusion, SIAD is one of the causes of ischemic stroke and TIA in young adults and characteristic clinical manifestations and follow-up MRA have a great diagnostic importance. The development of SIAD appears to be related to weakness of connective tissue of arterial wall.
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PMID:[Spontaneous intramural intracranial artery dissection and ischemic stroke]. 1819 22


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