Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve out of 49 patients with single or multiple transient ischemic attacks (TIAs) had TIA-related headaches, mostly in close temporal relation to the ischemic onset. Headache predominated in patients taking vasodilators when TIA occurred or with orthostatic hypotension at the first clinical examination, but atrial hypertension or a personal history of migraine were not more frequent in patients with headache. The site of the pain did not correlate with the presumed territory of cerebral ischemia. Pain during TIA is conceivably due to an interaction between cerebral vessels and the surrounding nervous system. Blood vessels have a sturdy physiological role concerning blood flow regulation, with receptors and signaling molecules potentially involved with pain production. Reflex mechanisms should justify pain in other areas.
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PMID:On the pathogenesis of headache following TIA. 962 73

Right-to-left shunt (RLS), usually due to patent foramen ovale, is a well-established risk factor for ischemic stroke in young patients, while the role of migraine as an independent factor is still debated. We evaluated 44 patients suffering from migraine with aura, and compared them with 73 patients younger than 50 with focal cerebral ischemia, and 50 controls, asymptomatic for cerebrovascular disease, and without a history of migraine. All the subjects underwent bilateral transcranial Doppler with injection of contrast medium in an antecubital vein. The test was performed during normal ventilation and during Valsalva maneuver, recording both the middle cerebral arteries and the basilar artery. Criteria for diagnosing RLS was the presence of at least 3 microbubbles within 15 s from injection. Eighteen out of 44 migraine patients (41%) showed RLS, as opposed to 8 of 50 controls (16%) (p < 0.005). Twenty-six out of 73 patients with cerebral ischemia had RLS (35%). We conclude that the prevalence of RLS in patients with migraine with aura is significantly higher than in normal controls, and is similar to the prevalence of RLS in young patients with stroke. These findings could be helpful in understanding the relationship between migraine and stroke.
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PMID:Migraine with aura and right-to-left shunt on transcranial Doppler: a case-control study. 977 49

Thrombosis, thrombocytopenia, recurrent fetal loss and a variety of non-thrombotic neurological disorders have all been associated with antiphospholipid antibodies (aPL). Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Depression, cognitive dysfunction, depression and psychosis have all been associated with aPL. The presumed pathophysiologic mechanism underlying these manifestations is thought to be a result of cerebral ischemia in some, but not all cases. Seizures, chorea and transverse myelitis all appear to be associated with aPL. An interaction between aPL and central nervous system cellular elements rather than aPL-associated thrombosis seems to be a more plausible mechanism for these clinical manifestations. Migraine on the other hand, does not appear to be associated with aPL in either lupus or non-lupus populations. Neuroimaging studies show an increased frequency of brain abnormalities in patients with aPL, but none appear to be specific. The best treatment strategy for preventing neurological manifestations of aPL is not fully defined. For thrombotic manifestations, both antiplatelet and anticoagulant therapies have been suggested. In some patients, immunosuppressant therapy has been used. For non-thrombotic manifestations, some combination of immunosuppressant therapy and symptomatic treatment may be warranted.
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PMID:Neurological manifestations of antiphospholipid antibody syndrome. 981 77

The authors report a patient with migraine in whom they measured brain oxygenation indirectly during a visual aura by means of T2-weighted MRI. An aura of left homonomous quadrantanopia was accompanied by increased T2-weighted contrast intensity of bilateral regions in the occipital cortex, and the red nucleus and substantia nigra bilaterally. The mechanisms of these changes remain to be determined, but in this patient the migraine aura was associated with probable hyperoxia and not cerebral ischemia.
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PMID:MRI of the occipital cortex, red nucleus, and substantia nigra during visual aura of migraine. 981 84

According to the trigeminovascular model of pain in migraine, sterile neurogenic inflammation of dural vessels stimulates nociceptive fibres of the trigeminal nerve. Sumatriptan, a 5-HT1 receptor agonist, blocks this reaction and mediates vasoconstriction of meningeal arteries. However, it is uncertain, whether sumatriptan also has a vasoconstrictive effect on cerebral arteries, which may influence vasoneuronal coupling and induce secondary cerebral blood flow changes. We studied changes of cerebral blood flow velocity (CBFV) and the pulsatility index (PI) in the posterior cerebral artery (PCA) after stimulus activation before, 10 min and 30 min after subcutaneous application of 6 mg sumatriptan, in order to assess potential vasoactive effects on cerebral circulation. CBFV was recorded from both PCAs simultaneously in 27 migraineurs (twenty women, seven men, mean age 29 years), and arterial blood pressure (BP), heart rate (HR) and respiration rate (RR) were monitored. Although the mean diastolic blood pressure rose significantly from 75 mm Hg to 81 mm Hg (P<0.05) and systolic blood pressure and respiration rates remained constant, average CBFV values remained constant. Similarly, the relative increase of CBFV by visual stimulation, which is clearly higher compared to controls in other studies (55.0% before, 52.6% after 10 min, and 52.4% after 30 min), and absolute mean values for CBFV and PI did not change after visual stimulation. These results provide evidence against the hypothesis that sumatriptan produces vasoconstriction in the intracranial human arterial circulation as a potential risk of cerebral ischemia.
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PMID:Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCD study. 1050 Feb 62

With recent developments in current density imaging (CDI), it is feasible to utilize this new technique in brain imaging applications. Since CDI's ability to measure changes in current density depends on a concomitant activity-dependent change in the conductivity of the brain tissue, we have examined the changes in complex conductivity during spreading depression (SD) in rodent neocortex using a coaxial probe. SD was chosen because it is often referred to as an animal model of cerebral ischemia and migraine with aura. The conductivity measurements revealed a change with short latency (30-60 s) followed by a change with a longer latency (200-300 s). This change in conductivity with short latency has not been reported before, and we conjecture that it may be the priming or triggering mechanism prior to the main SD episode. A 20% change in conductivity during SD is sufficiently large to be measured by CDI. Therefore, the ability to measure changes in the conductivity, as opposed to metabolic changes, makes CDI a viable approach to the study of ischemia and migraine with aura.
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PMID:Changes in the complex permittivity during spreading depression in rat cortex. 1058 18

Modern molecular biology has revealed vast numbers of large and complex proteins and genes that regulate body function. By contrast, discoveries over the past ten years indicate that crucial features of neuronal communication, blood vessel modulation and immune response are mediated by a remarkably simple chemical, nitric oxide (NO). Endogenous NO is generated from arginine by a family of three distinct calmodulin- dependent NO synthase (NOS) enzymes. NOS from endothelial cells (eNOS) and neurons (nNOS) are both constitutively expressed enzymes, whose activities are stimulated by increases in intracellular calcium. Immune functions for NO are mediated by a calcium-independent inducible NOS (iNOS). Expression of iNOS protein requires transcriptional activation, which is mediated by specific combinations of cytokines. All three NOS use NADPH as an electron donor and employ five enzyme cofactors to catalyze a five-electron oxidation of arginine to NO with stoichiometric formation of citrulline. The highest levels of NO throughout the body are found in neurons, where NO functions as a unique messenger molecule. In the autonomic nervous system NO functions NO functions as a major non-adrenergic non-cholinergic (NANC) neurotransmitter. This NANC pathway plays a particularly important role in producing relaxation of smooth muscle in the cerebral circulation and the gastrointestinal, urogenital and respiratory tracts. Dysregulation of NOS activity in autonomic nerves plays a major role in diverse pathophysiological conditions including migraine headache, hypertrophic pyloric stenosis and male impotence. In the brain, NO functions as a neuromodulator and appears to mediate aspects of learning and memory. Although endogenous NO was originally appreciated as a mediator of smooth muscle relaxation, NO also plays a major role in skeletal muscle. Physiologically muscle-derived NO regulates skeletal muscle contractility and exercise-induced glucose uptake. nNOS occurs at the plasma membrane of skeletal muscle which facilitates diffusion of NO to the vasculature to regulate muscle perfusion. nNOS protein occurs in the dystrophin complex in skeletal muscle and NO may therefore participate in the pathophysiology of muscular dystrophy. NO signalling in excitable tissues requires rapid and controlled delivery of NO to specific cellular targets. This tight control of NO signalling is largely regulated at the level of NO biosynthesis. Acute control of nNOS activity is mediated by allosteric enzyme regulation, by posttranslational modification and by subcellular targeting of the enzyme. nNOS protein levels are also dynamically regulated by changes in gene transcription, and this affords long-lasting changes in tissue NO levels. While NO normally functions as a physiological neuronal mediator, excess production of NO mediates brain injury. Overactivation of glutamate receptors associated with cerebral ischemia and other excitotoxic processes results in massive release of NO. As a free radical, NO is inherently reactive and mediates cellular toxicity by damaging critical metabolic enzymes and by reacting with superoxide to form an even more potent oxidant, peroxynitrite. Through these mechanisms, NO appears to play a major role in the pathophysiology of stroke, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis.
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PMID:Endogenous nitric oxide synthesis: biological functions and pathophysiology. 1063 Jun 82

Neurological diseases during and following pregnancy represent a small subgroup of all neurological diseases. They can be divided into three groups. 1) Diseases which existed already before pregnancy or which appear just by chance during this phase like migraine, multiple sclerosis, myasthenia gravis, epilepsy, brain tumors or Guillain-Barre syndrome. 2) Diseases that can appear without pregnancy but which display a higher incidence in connection with pregnancy. Cerebral ischemia, intracerebral hemorrhage, subarachnoidal hemorrhage, intracranial venous thrombosis and compression neuropathies belong to this group. 3) Preeclampsia/eclampsia, HELLP syndrome, amniotic fluid embolism and pituitary apoplexy are diseases with neurological symptoms which occur only with pregnancy. The pregnancy itself can imply some restrictions or even a contraindication concerning diagnosis and therapy of these diseases. The decision in favour or against diagnostic or therapeutic approaches is determined by possible effects on the fetus and by potential danger resulting from not recognizing or not treating such a disease.
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PMID:[Neurologic diseases and pregnancy]. 1063 11

Recent evidence suggests that reproductive steroids are important players in shaping stroke outcome and cerebrovascular pathophysiologic features. Although women are at lower risk for stroke than men, this native protection is lost in the postmenopausal years. Therefore, aging women sustain a large burden for stroke, contrary to a popular misconception that cancer is the main killer of women. Further, the value of hormone replacement therapy in stroke prevention or in improving outcome remains controversial. Estrogen has been the best studied of the sex steroids in both laboratory and clinical settings and is considered increasingly to be an endogenous neuroprotective agent. A growing number of studies demonstrate that exogenous estradiol reduces tissue damage resulting from experimental ischemic stroke in both sexes. This new concept suggests that dissecting interactions between estrogen and cerebral ischemia will yield novel insights into generalized cellular mechanisms of injury. Less is known about estrogen's undesirable effects in brain, for example, the potential for increasing seizure susceptibility and migraine. This review summarizes gender-specific aspects of clinical and experimental stroke and results of estrogen treatment on outcome in animal models of cerebral ischemia, and briefly discusses potential vascular and parenchymal mechanisms by which estrogen salvages brain.
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PMID:Estrogen as a neuroprotectant in stroke. 1077 8

Moyamoya disease is a cerebrovascular disease with progressive occlusion of both internal carotid arteries and of their branches and formation of a new vascular network at the base of the brain. Because of the angiographic appearance, it is named as moyamoya. The clinical features are cerebral ischaemia, recurrent transient ischaemic attacks, sensorimotor paralysis, convulsions and migraine-like headaches. A 10-year-old child who acutely developed hemiparesis, weakness and aphasia was found to have moyamoya disease and heterozygous protein S deficiency. This case shows us that during the thromboembolic events the coexistence of protein S deficiency and moyamoya should be investigated.
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PMID:Moyamoya syndrome with protein S deficiency. 1100 63


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