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)

Recombinant gamma interferon (rHuIFN-gamma) has been recognized to increase mRNA and protein levels of C1 inhibitor (C1 INH) in various human cells. Further, when administered to patients with colon cancer, it increased plasma C1 INH levels. A prospective trial was initiated to determine whether rHuIFN-gamma could elevate plasma C1 INH levels in six normal volunteers and two patients with type I angioedema. After 1 month of observation of plasma C1 INH levels, rHuIFN-gamma was administered subcutaneously at 25 micrograms/M2 daily for 4 consecutive days. All healthy volunteers and patients experienced local erythema, headache, myalgias, and chills during the administration of rHuIFN-gamma. C1 INH, prekallikrein, high-molecular-weight kininogen, and factor XII levels in plasma were not influenced by the rHuIFN-gamma administration. One patient with hereditary angioedema (HAE) had an attack of angioedema 3 days after completion of rHuIFN-gamma therapy. During the attack, circulating cleaved high-molecular-weight kininogen, kallikrein-alpha 2-macroglobulin complexes, and an altered 50 kd form of kallikrein were detected in the patient's plasma. Additional studies showed that rHuIFN-gamma treatment resulted in decreased total fibrinolytic activity. It was found that immediately after rHuIFN-gamma treatment, tissue plasminogen activator activity and antigen levels were not significantly decreased in volunteers. Plasminogen activator inhibitor levels rose significantly, but this activity was not due to plasminogen activator inhibitor-1 antigen, whose value significantly fell. These data suggest that rHuIFN-gamma may stimulate the expression of another plasminogen activator inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Administration of gamma interferon in human subjects decreases plasminogen activation and fibrinolysis without influencing C1 inhibitor. 830 Nov 99

Vasotropic, haemostatic and haemorheological parameters have been investigated in 17 patients suffering from migraine without aura in comparison with 11 sex and age matched healthy control subjects. NO metabolites (NO2- and NO3-), endothelin (ET-1), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), fibrinogen, D-dimer, fibrinopeptide A, beta thromboglobulin (beta-TG), blood viscosity, plasma viscosity, haematocrit (Htc) and red blood cell (RBC) filterability index (FI) were determined during headache free periods. Migraineurs NO3- and ET-1 plasma levels, compared to control values, showed a significant decrease and increase respectively; fibrinogen, beta-TG and D-dimer appeared slightly lowered in migraineurs, while Htc remained in the normal limits; tPA, PAI-1 and FI were significantly reduced, while fibrinopeptide A, blood viscosity and plasma viscosity at a low shear rate (shr) exhibited a significant rise. Data obtained support the involvement of endothelial, haemostatic and haemorheological functions in the pathogenesis of migraine.
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PMID:Endothelial, haemostatic and haemorheological modifications in migraineurs. 886 51

Cervicocranial arterial dissection (CCAD) occurs when there is a tear in the intimal layer of the carotid or vertebral arteries with subsequent extravasation of blood into the subintimal layers. The dissection may be extradural, intradural, or extend over both segments. The contents of the subintimal layers are highly thrombogenic, and thus, embolism, vessel stenosis, or occlusion may follow. Symptoms of dissection may be caused by local injury to the blood vessel or by ischemia to the retina or brain. Thus, dissection should always be considered in patients who present with Horner syndrome associated with ipsilateral headache, carotidynia, ocular pain, or amaurosis fugax. Rare neuro-ophthalmologic presentations of dissection include anterior and posterior ischemic optic neuropathy; central retinal artery occlusion; ophthalmic artery occlusion; transient ophthalmoparesis; and third, fourth, or sixth cranial nerve palsy. The most common serious complication of dissection is ischemic stroke. No randomized controlled trials have evaluated therapies for patients presenting with CCAD. Thus, treatment is essentially empiric and often varies by region. Medical management is first line in most patients. Given the propensity for thrombus formation and early embolization or occlusion, acute anticoagulation using intravenous heparin or low-molecular-weight heparinoids followed by short-term, dose-adjusted warfarin is the treatment of choice for most patients with extradural CCAD who present early after symptom onset. The risk of cerebral ischemia is greatest in the first few weeks after dissection; thus, it is reasonable to recommend antiplatelet agents for patients who present late and have not had evidence of ischemia. Intradural dissection is rare but is associated with a meaningful risk of subarachnoid hemorrhage (SAH). As a result, anticoagulants and antiplatelet agents should not be used if SAH is suspected or confirmed. Endovascular intervention may be necessary in a small minority of cases with recurrent events despite anticoagulation or SAH due to intradural dissection. Of special note, CCAD is not considered a contraindication for tissue plasminogen activator use in acute stroke patients who are otherwise eligible for treatment.
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PMID:Cervicocranial arterial dissection. 1728 90

Cerebral hyperperfusion and reperfusion injuries are not infrequently encountered following in reperfusion of ischemic or hypoperfused brain. Mechanism of injury could be related to tissue plasminogen activator toxicity, oxidative stress, and hyperperfusion due to impaired cerebral autoregulation in already maximally dilated cerebral vasculature and compromised cerebral hemodynamic reserve. Reperfusion injury can present as headaches and seizures in mild forms and as subarachnoid hemorrhage, intracranial hemorrhage, cerebral edema, and encephalopathy in its most severe manifestation. Prevention and identifying those at risk of hyperperfusion syndromes are the best strategy. Active treatment includes basic neurocritical care with reduction of blood pressure to a reperfused brain and timely neuroprotection and cerebral edema control measures are the mainstay of its management approach.
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PMID:Neurocritical care of a reperfused brain. 2104 86

We present a case of middle cerebral artery (MCA) dissection that was treated with intravenous administration of recombinant tissue plasminogen activator (rt-PA). A 72-year-old woman suddenly developed dysarthria and left motor weakness without headache. On arrival at the hospital, her NIH stroke scale (NIHSS) score was 13. Magnetic resonance imaging (MRI) revealed severe stenosis of the right proximal MCA segment; this appeared to be the cause of atherothrombosis. After the MRI study, her NIHSS score improved to 5, but the evidence of MCA stenosis indicated the need for thrombolytic treatment. We injected rt-PA 102 min after the symptom onset; however, her NIHSS score fluctuated thereafter; at worst, it was 13 at 78 min after the initiation of rt-PA treatment. Eventually, her neurological status improved and after 12 hours, her NIHSS score improved to 1 but the MRI showed cerebral infarction restricted in the right putamen. Since persistent irregularity of the right MCA was shown by follow-up magnetic resonance angiography (MRA), digital subtraction angiography was performed on the 14th day after admission. Double lumen of the right MCA was detected, which was a definite proof of artery dissection. Here, we discuss the difficulties encountered in the diagnosis and treatment for MCA dissection.
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PMID:[Middle cerebral artery dissection treated with intravenous tissue plasminogen activator injection: a case report]. 2137 37

Cerebral venous thrombosis is a rare but potentially severe condition in children. We present the case of a teenager with corticodependent nephrotic syndrome diagnosed at five months of age and treated with cyclosporine A. In the context of recurrence of nephrotic syndrome he presented with headache, vomiting and severe intracranial hypertension. While the raised intracranial pressure and the status epilepticus were controlled, the brain imaging revealed venous thrombosis of all venous sinus, with absence of venous drainage. He was submitted to local thrombolysis with recombinant tissue plasminogen activator, with recanalization of the venous sinuses. The outcome was favourable, without neurological deficits. In this case, the early radiologic intervention was crucial, enabling a full neurological recovery, in a teenager whose initial prognosis was very poor.
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PMID:[Endovascular thrombolysis for massive cerebral venous thrombosis in a teenager with nephrotic syndrome]. 2162 91

Cerebral venous thrombosis (CVT) is a potentially serious disease, with nonspecific clinical symptoms and an unpredictable outcome. Despite adequate anticoagulation, a patient's clinical condition can rapidly deteriorate. The aim of this study was to evaluate the efficacy of local thrombolysis in these patients. Consecutive patients with progressive cerebral venous thrombosis between October 2008 and January 2011 were enrolled prospectively. Progressive CVT was defined as the persistence of neurologic findings (headache, blurred vision, and visual field defects) despite at least four days (or 48 hours in patients with involvement of more than one sinus) on full anticoagulation therapy with heparin and development of focal neurologic deficits or cortical hemorrhage. We excluded patients with large hematomas and predisposing malignancies like leukemia. All patients underwent local thrombolysis with 30 mg recombinant tissue plasminogen activator (rtPA). Overall, 26 patients were enrolled with a mean age of 35.5 years (range 18 to 56 years). Six patients (23%) were male and twenty patients (77%) were female. The most common presenting feature was headache and the most common neurologic finding was papilledema, which was present in all patients. Eighty-five percent of women had a history of oral contraceptive pill consumption. Successful recanalization was achieved in all patients except one (96.2%). Neurological examinations and follow-up assessments were based on a modified Rankin scale (mRS). Favorable outcome and recovery was defined as a mRS score of 0-1. Follow-up assessments at the third week showed that 25 out of 26 recovered, with 18 having a mRS score of 0 and 7 with a mRS score of 1. There were no procedure-related neurological complications. Our results show that local thrombolysis is a safe and effective treatment modality for patients suffering from progressive CVT.
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PMID:Treatment of progressive cerebral sinuses thrombosis with local thrombolysis. 2244 Jun 6

A 20-year-old woman was admitted to a Gynecology Hospital in her 6(th) month of pregnancy for high blood pressure and tonic-clonic seizure. Primary diagnosis was eclampsia, and for that reason she underwent cesarean section. She also had headache on frontal and parietal areas without nausea or vomiting. There was not a focal neurological sign. Rheumatology consultation was requested. Systemic lupus erythematosus and secondary antiphospholipid (APS) was confirmed. The patient had headache that continued several days after cesarean section, therefore, brain magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) were performed, and cerebral vein thrombosis was documented. Distal segment of right lateral sinus and sigmoid sinus were not appeared in brain MRV. Abnormal hypersignal intensity of right lateral sinus/coronal T2 was detected. Thrombolytic therapy with 20 mg tissue plasminogen activator on right sigmoid and transverse sinus was performed by an interventional neurologist. After this procedure, the patient(')s headache healed and she was discharged in a good condition.
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PMID:Thrombolytic therapy for cerebral vein thrombosis in antiphospholipid syndrome secondary to systemic lupus erythematosus. 2311 32

Intravenous (IV) thrombolysis is approved and proven treatment for acute ischemic stroke in the window period of 4.5 hours. The therapeutic benefit is not extended to many patients with prior stroke and recurrent stroke as they are excluded in the protocol for thrombolysis. We report a case of successful IV thrombolysis in a young patient with recent prior stroke and recurrent stroke. A 35-year-old male presented in our emergency with recurrent stroke had a history of acute onset vertigo, headache, and vomiting. He was diagnosed to have posterior circulation stroke before 5 days on the basis of clinical history and neuroimaging. On the day of presentation to our hospital, he had developed new symptom of acute onset right hemiparesis with dysarthria. IV tissue plasminogen activator administered within 2 hours of onset of new symptoms resulted in significant improvement in spite of the recent prior stroke.
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PMID:Thrombolysis in recurrent stroke-beyond guidelines: a case report. 2508 67

A 41-year-old woman was admitted due to a sudden-onset severe headache, left hemiparesis and dysarthria. Diffusion-weighted magnetic resonance imaging showed an acute infarct in the bilateral pons, and magnetic resonance angiography revealed basilar artery (BA) occlusion resulting from dissection of the right vertebral artery (VA). She was treated with intravenous recombinant tissue plasminogen activator (rt-PA) 110 minutes after symptom onset. Subsequently, brain angiography was performed along with mechanical thrombolysis using Trevo ProVue retriever devices. The BA was successfully recanalized 240 minutes after the onset of symptoms. Thrombectomy is a promising treatment strategy for cases of VA dissection resistant to intravenous rt-PA thrombolysis.
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PMID:Thrombectomy using Trevo ProVue Stent Retriever Devices after Recombinant Tissue Plasminogen Activator Thrombolysis for Acute Basilar Artery Occlusion during Vertebral Artery Dissection. 2708 17


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