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)

Iloprost is a synthetic stable analogue of prostacyclin (PGI2), which shares its antiaggregating and vasodilating properties. Iloprost has been administered by i.v. route to patients with critical limb ischaemia (CLI) of different origin (maximal dosage: 2 ng/kg/min 6 hours/day infusion for 14-28 days). In patients with claudicatio intermittens (Fontaine stage II) iloprost improved the time to claudication and the maximal walking distance on treadmill, with an effect still lasting 60 days after suspension. This benefit was not related to a significant improvement in blood flow. Five multicentric, perspective, randomized versus placebo studies in patients with more severe CLI (Fontaine stage III-IV) susceptible to surgical treatment, showed that iloprost was able to reduce pain and ulcer dimensions. Furthermore, tha amputation rate of the ischemic limb was significantly lower in patients treated with iloprost during a 6 month follow-up (p < 0.01). Iloprost was also more effective than aspirin in causing pain relief and ulcer healing in patients with thromboangiitis obliterans and more effective than nifedipine in reducing frequency, intensity and duration of ischemic episodes in patients with Raynaud's phenomenon. Minor side effects of iloprost administration are represented by facial flushing, tachycardia, headache, nausea, vomiting, abdominal cramping, diarrhoea, whose frequency ranges from 16% to 70%; major collateral effects, occurring in less than 5% of patients, are above all represented by severe hypotension and angina pectoris. Clinical data indicate therefore that iloprost treatment can allow to improve the clinical conditions and the prognosis in patients with critical ischemia of the limbs, not candidate to surgical revascularization, by causing a relief of pain, a reduction in ulcer dimensions and deferring amputation.
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PMID:[The role of iloprost in the treatment of critical ischemia of the limbs]. 750 14

Lower limb critical ischemia is a clinical condition typical of patients with severe chronic obstructive arterial disease (Fontaine's IIIb and IV degree). This condition often leads to amputation of the limb involved. The authors present to the use PGE1 in 50 patients with Fontaine's IIIb-IV degree chronic obstructive arterial disease of lower limbs in which the indication of amputation was done. All the patients, admitted to the emergency ward, complain of rest pain and distal ulcers. The administration of PG5(1) was given as follows: 40 mg/bid/e.v./20 days. A 6 months long follow-up was installed with the instrumental evaluation of: Transcutaneous oxygen pressure; Distal blood perfusion with Doppler; cardiac pulse; blood pressure. Eighteen patients became to a Fontaine's II degree during the next 2 months after therapy, 25 patients came back to a severe claudicatio: of them 18 underwent successfully vascular surgery, 7 underwent amputation of the lower limb. In 7 patients the PGE1 did not influence the natural progression of the disease. Among the side-effects of therapy we can mention: headache (4%), erythema and pain of injected vein (8%), sick (4%). All the side effects were transient and never led to interruption of therapy.
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PMID:[Use of PGE1 in severe ischemia of the lower extremities. Clinical study]. 756 37

31-phosphorus Magnetic Resonance Spectroscopy (MRS) is a technique developed for the non-invasive study of energy metabolism in living subjects. It determines the concentrations of high and low energy phosphates in resting and activated conditions, and of intracellular pH. 31P-MRS has been applied to the study of migraine, both during and in between attacks. Intracellular brain pH remains unchanged during the migraine attack, suggesting that ischemia does not play a relevant role in the origin of the neurological signs. During and in-between attacks, migraineurs display abnormalities in energy metabolism of brain and muscle, consisting of reduced levels of phosphocreatine, reduced cellular-free energy and increased rate of ATP biosynthesis. We suggest that these abnormalities in energy metabolism predispose migraineurs to develop an attack under conditions of increased brain energy demand.
Cephalalgia 1995
PMID:Magnetic resonance spectroscopy in migraine. 758 31

Migraine pain has traditionally been ascribed to dilatation of primarily extracranial arteries. Such dilatation has, however, not been demonstrated so far. Studies of microcirculation reveal no major hyperperfusion or ischemia in the temporal muscle or the subcutaneous tissue in the temporal region during attacks of migraine. However, a reduction in the orthostatic reactivity of the subcutaneous arterioles was observed on the side of the headache. Increased tenderness of the pericranial myofascial tissues is observed during migraine attacks, particularly on the side of the headache. Increased tension of pericranial muscles on the other hand is not a constant finding and migraine attacks are not induced by experimentally increased tension of the temporal and masseter muscles. Extracranial pain and tenderness may, however, be induced experimentally by intramuscular injections of hypertonic saline and potassium chloride as well as of endogenous substances like bradykinin with 5-hydroxytryptamine and bradykinin with substance P. The extracranial arteries and myofascial structures are both supplied by unmyelinated trigeminal sensory nerve fibers containing a variety of neuropeptides which are released during migraine attacks. Axonal reflexes between extracranial arteries and neighbouring myofascial tissues as well as referred pain mechanisms may account for the observed tenderness during migraine attacks.
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PMID:Extracranial blood flow, pain and tenderness in migraine. Clinical and experimental studies. 769 38

These experiments were designed to investigate a possible mechanism linking the phenomenon of cortical spreading depression with activation of the trigeminal sensory system in migraine. Blood flow in the cortex and middle meningeal artery was measured in cats before and during propagation of a wave of cortical spreading depression, initiated by cortical pin-prick. This caused a transient propagated increase in cortical blood flow. Cortical spreading depression was accompanied by a decrease in blood flow in the middle meningeal artery, sometimes to very low levels. The results suggest that the pain of migraine could arise from dural ischemia induced by cortical spreading depression.
Cephalalgia 1994 Dec
PMID:Cortical spreading depression reduces dural blood flow--a possible mechanism for migraine pain? 769 4

Most shunt-dependent hydrocephalic patients present with predictable symptoms of headache and mental status changes when their cerebrospinal fluid shunts malfunction. Their intracranial pressure (ICP) is usually high, and they usually respond to routine shunt revision. This report describes 12 shunted patients who were admitted with the full-blown hydrocephalic syndrome but with low to low-normal ICP. All 12 patients had been maintained previously on medium-pressure shunts. Their symptoms included headache, lethargy, obtundation, and cranial neuropathies. At peak symptoms, their ventricular sizes were large (ventricular/biparietal ratio of 0.35 to 0.45) in six and massive (ventricular/biparietal ratio > 0.45) in six and their ICPs ranged from 2.2 to 6.6 mm Hg, with a mean of 4.4 +/- 1.3 mm Hg (+/- standard deviation), i.e., below or well within the pressure range of their shunts. The pressure volume index of three patients at peak symptoms ranged from 39.2 to 48.5 ml, with a mean of 43.9 +/- 4.6 ml, which represents a 190% increase from the predicted normal value. Seven patients failed to improve with multiple shunt revisions, including the use of low-pressure valves. In 11 patients, symptoms and ventriculomegaly were not reversed except with prolonged external ventricular drainage at subzero pressures (mean external ventricular drainage nadir pressure of -5.7 +/- 3.6 mm Hg, for a mean period of 22.2 days). During external ventricular drainage treatment, symptoms correlated only with ventricular size and not with ICP. All 11 were subsequently treated successfully with a new medium- or low-pressure shunt. One patient was treated successfully with prolonged shunt pumping. We postulate that: 1) the development of this low-pressure hydrocephalic state is related to alteration of the viscoelastic modulus of the brain, secondary to expulsion of extracellular water from the brain parenchyma, and to structural changes in brain tissues due to prolonged overstretching; 2) certain patients are susceptible to developing low-pressure hydrocephalic state because of an innate low brain elasticity due to bioatrophic changes; 3) low-pressure hydrocephalic state symptoms are due not to pressure changes but to brain tissue distortion and cortical ischemia secondary to severe ventricular distortion and elevated radial compressive stresses within the brain; and 4) treatment must be directed toward allowing the entry of water into the brain parenchyma and the restoration of baseline brain viscoelasticity.
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PMID:Low-pressure hydrocephalic state and viscoelastic alterations in the brain. 780 7

Moyamoya disease is a cerebrovascular disease characterized radiologically by progressive narrowing and occlusion of the arteries contributing to the circle of Willis and its branches. There is formation of an exuberant collateral network of blood vessels at the base of the brain, which is thought to arise in response to chronic ischemia. Clinically, the course is variable, with patients having repeated transient ischemic attacks, strokes, migraine, and seizures. Effective treatment is not available. The etiology and pathophysiology of moyamoya disease are largely unknown. Two patients with arteriographically proven moyamoya disease were identified. Both patients were symptomatic before age 5 years. Despite successful encephaloduroarteriosynangiosis revascularization procedures, they continued to experience an inexorable downhill course. A calcium channel blocker (nicardipine HCl) was introduced in order to prevent further symptoms. After the introduction of nicardipine, no further strokes occurred in either patient. There were no further episodes of transient ischemic attacks, seizures, or headache in one patient and decreased frequency in the other. In patients with moyamoya disease, nicardipine may have a beneficial effect on cerebral hemodynamics and may prevent ischemic sequelae by optimizing existing collateral circulation.
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PMID:Use of a calcium channel blocker (nicardipine HCl) in the treatment of childhood moyamoya disease. 782 27

Localized 1H magnetic resonance spectroscopy was performed in a 45-year-old woman with migraine. She developed throbbing headache attacks without aura since thirteen years ago and the attack was accompanied with right hemiplegia since seven years ago. Brain MRI showed no abnormalities and 123I-IMP SPECT revealed mild frontal dominant decrease of cerebral blood flow. It seemed that her condition was positioned between migraine with prolonged aura and migrainous infarction of complicated migraine in the classification of International Headache Society. Spectra obtained from bilateral frontal lobe interictally showed elevation of lactate at left side. Choline, creatine, and N-acetyl-aspartate were almost equal on both side. The above results suggest that slight ischemia which is not detected by MRI is present or there is a disturbance of oxidative glycolysis, which is induced by mitochondrial dysfunction.
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PMID:[Elevation of cerebral lactate detected by localized 1H magnetic resonance spectroscopy in a patient with migraine]. 792 68

In a series of 102 patients with angiographically proven cerebral sinus venous thrombosis (SVT) significant differences with arterial cerebrovascular disease were noted with respect to disease onset, reversibility of symptoms, occurrence of epileptic seizures and headache, cerebral blood flow under resting and stimulated conditions, occurrence of intracranial bleedings, and response to heparin therapy. From these findings pathophysiological differences are hypothesized: Whereas arterial cerebral ischemia usually is a monophasic abrupt thrombotic process and there is only a small penumbra, SVT is a continuing process of disequilibrium between prothrombotic and thrombolytic mechanisms; large areas of the brain are only functionally or metabolically disturbed but not irreversibly damaged. Intracranial bleeding in SVT is a consequence of increased venous and capillary pressure and thus occurs more frequently than in arterial thrombotic disease in which capillary pressure is reduced by the thrombosis and bleeding occurs during reperfusion of tissue damaged by ischemia. Heparin treatment in SVT is effective since it shifts the equilibrium away from the prothrombotic side and is able to save large areas of brain tissue that are only reversibly damaged. It improves venous outflow and thus decreases the risk of intracranial hemorrhage, in contrast with the arterial thrombotic disease where heparin increases the risk or at least the severity of intracranial bleedings.
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PMID:Pathophysiological aspects of cerebral sinus venous thrombosis (SVT). 801 60

We report the clinical findings and stroke mechanisms of 63 patients with cerebellar infarcts. We divided the intracranial vertebrobasilar circulation into the proximal territory (P), fed by the intracranial vertebral arteries and their branches; the middle territory (M), fed by the proximal and middle basilar artery and its branches; and the distal territory (D), fed by the rostral basilar artery and its branches. Cerebellar infarcts were classified by vascular territories P, M, D, P&D, and middle-plus (P&M, M&D, and P&M&D). Patients with P infarcts (11 patients) frequently had vertigo, gait instability, limb ataxia, and headache, whereas patients with D infarcts (15 patients) most often had limb ataxia, gait instability, and dysarthria. Patients with P&D infarcts (17 patients) had signs and symptoms of both groups combined. Infarcts in which the middle territory was involved, either alone (three patients) or combined with other territories (17 patients) were dominated by brainstem signs and symptoms. The predominant stroke mechanisms in the P, D, and P&D groups were embolic due to intra-arterial or cardiac embolism. When the M territory was involved, either alone or with P, D, or P&D territories, stroke mechanisms were more varied, and there was often large-artery occlusion with hemodynamic ischemia.
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PMID:Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. 805 34


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