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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 130 obstetrical patients were treated with either low molecular weight (LMW) or unfractionated (UFH) heparin as part of prospective study comparing their efficacy in the prevention of thromboembolism. A single daily dose of 2500-5000 anti-Xa-units LMW heparin (Fragmin) or two to three daily doses of 5000 IU UFH (Liquemin) were given to two groups of 15 patients with therapeutic tocolysis and 50 patients with cesarean section. Patients with cesarean section were given 500 ml Dextran 60 i.v. during surgery followed by subcutaneous injection of heparin eight to ten hours after surgery. Heparin therapy was continued for ten days after surgery. None of the patients exhibited clinical signs of thrombosis. The majority of patients showed symptoms of local irritation at the site of heparin injection (69% of patients with LMW heparin; 80% of patients with UFH). Hematomas at the site of injection were significantly smaller when LMW heparin was used instead of UFH. A number of patients experienced headache after heparin application (10% of patients with LMW heparin; 13% of patients with UFH). There were no cases of post surgical haemorrhage. Comparison of daily profiles revealed a significantly higher anti-Xa-activity of LMW heparin compared to UFH. In contrast, other coagulation parameters were not different in the two experimental groups (antithrombin III, partial thrombin time, thrombin time). Hematologic parameters and liver enzymes were in the physiological range in both experimental groups and none of the patients exhibited signs of heparin induced thrombocytopenia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of thromboembolism with low molecular weight heparin (Fragmin) in obstetrics]. 797 97

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

Carotid-cavernous aneurysms account for between 1.9% and 9.0% of intracranial aneurysms. Entirely intercavernous aneurysms are believed to have a relatively benign course, with cranial nerve findings or headache being the usual initial symptomatology; however, subarachnoid hemorrhage or carotid-cavernous fistula formation can result from rupture. Over the past 15 years endovascular parent artery occlusion has essentially replaced surgical carotid occlusion as the treatment of choice. The authors describe a series of 39 consecutive patients at the University of Virginia Health Sciences Center who underwent endovascular treatment of a carotid-cavernous aneurysm. Aggressive invasive hemodynamic monitoring and maintenance of a state of normo- to mild hypervolemia in the asymptomatic patient was used throughout the periprocedural period. Rapid institution of hypervolemic-hypertensive therapy can reverse early neurological deficits related to hypoperfusion in these patients. Only one individual managed with this protocol developed neurological deficits not reversible with hypertensive-hypervolemic therapy. Heparin therapy was administered for 48 hours after occlusion, with patients receiving subsequent aspirin therapy for 6 months to combat distal embolism secondary to thrombosis. Long-term complications were not seen in patients receiving aneurysm trapping; however, two individuals with proximal carotid occlusion developed late optic neuropathy and one had recurrent transient ischemic attacks that ceased with supraclinoidal carotid clipping.
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PMID:Medical management in the endovascular treatment of carotid-cavernous aneurysms. 862 48

Carotid artery dissection is a major cause of cerebral infarction in the young. The extracranial portion of the internal carotid artery is much more frequently involved than the intracranial portion. In up to 20% of cases it is bilateral or associated with vertebral artery dissection. It is mainly characterised by local signs such as headache or facial pain, Horner's syndrome, lower cranial nerve palsies and pulsatile tinnitus, followed a few hours or days later by signs of cerebral or retinal ischemia. Ultrasound investigations show signs of distal stenosis or occlusion, highly suggestive of dissection, but the best diagnostic tool is presently the association of magnetic resonance imaging (MRI) and MR angiography which tend to replace intra-arterial angiography. The prognosis is highly variable: excellent in cases limited to local signs, but very poor leading to death or major sequelae in about 15% of cases. Various treatments have been suggested but no controlled trial has ever been performed in this condition. Heparin in the acute stage followed by warfarin or aspirin for 3 to 6 months is most commonly used.
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PMID:Internal carotid artery dissection: an update. 951 74

We report a 20-year-old woman who suffered headaches before presenting with a state of fluctuating vigilance. MRI showed diffuse high signal in the basal ganglia bilaterally on diffusion- and T2-weighted images, which had areas of both low and high apparent diffusion coefficient, presumed to correspond to cytotoxic and vasogenic oedema. MR venography showed no flow in the deep cerebral veins or straight sinus. Heparin was given, with clinical recovery. On follow-up MRI, the appearances became normal.
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PMID:Diffusion-weighted MRI suggests the coexistence of cytotoxic and vasogenic oedema in a case of deep cerebral venous thrombosis. 1111 73

We reviewed the haemorrhagic complications of the endovascular treatment of intracranial aneurysms, in terms of frequency, pre-embolisation clinical status, clinical and radiological manifestations, management and prognosis. In 275 patients treated for 303 aneurysms over 7 years we had seven (one man and six women--2.3%) with haemorrhage during or immediately after endovascular treatment. All procedures were performed with a standardised protocol of heparinisation and anaesthesia. Four had ruptured aneurysms, two at the tip of the basilar artery, and one ach on the internal carotid and posterior cerebral artery, treated after 12, 5, 14, and 2 days, respectively, three were in Hunt and Hess grade 2 and one in grade 1. Bleeding occurred during coiling in three, after placement of at least four coils, and during manipulation of the guidewire to enter the aneurysm in the fourth. Haemorrhage was manifest as extravasation of contrast medium, with a sudden rise in systolic blood pressure in three patients. The other three patients had unruptured aneurysms; they had stable blood pressure and angiographic findings during the procedure, but one, under sedation, had seizures immediately after insertion of four coils, and the other two had seizures, headache and vomiting on the day following the procedure. Heparin reversal with protamine sulphate was started promptly started when bleeding was detected in four patients, and the embolisation was completed with additional coils in three. Emergency ventricular drainage was performed in the two patients with ruptured aneurysm and one with an unruptured aneurysm who had abnormal neurological responses or hydrocephalus. The bleeding caused a third nerve palsy in one patient, which might have been due to ischaemia and progressively improved.
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PMID:Procedure-related haemorrhage in embolisation of intracranial aneurysms with Guglielmi detachable coils. 1285

The clinical picture of cerebral venous thrombosis (CVT) depends on the site of thrombosis in the venous system including superficial veins, deep veins and venous sinuses. Thrombotic changes may occur simultaneously in various parts of the venous system. Since CVT may have various causes, the knowledge of its etiology helps to make the diagnosis. In systemic diseases multiple intravascular clots may result, while in localized pathological conditions thrombosis maybe restricted to the lesion site. The clinical picture is often serious, leading to death, or to severe complications such as pulmonary embolism, and to distant complications--like epilepsy or intracranial hypertension being the cause of chronic headaches (lumbar puncture and CSF pressure measurement are helpful in the diagnosis of intracranial hypertension). In order to prevent complications of crucial importance is not only the proper diagnosis (with MRI and venography as the diagnostic techniques of choice), but also an early and prolonged treatment with anticoagulants. Heparin or fractionated heparin is recommended even though there is a possibility of cerebral haemorrhagic lesions.
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PMID:[Cerebral venous thrombosis--clinical aspects and consequences]. 1517 53

Cerebral venous thrombosis (CVT) is a rare type of cerebrovascular disease that can occur at any age, including in neonates, and it accounts for 0.5% of all stroke. The widespread use of neuroimaging now allows for early diagnosis and has completely modified our knowledge on this disorder. CVT is more common than previously thought and it is recognised as a non-septic disorder with a wide spectrum of clinical presentations, numerous causes, and usually a favourable outcome with a low mortality rate. MRI with T1, T2, fluid-attenuated inversion recovery, and T2* sequences combined with magnetic resonance angiography are the best diagnostic methods. D-dimer concentrations are raised in most patients but normal D-dimers do not rule out CVT, particularly in patients who present with isolated headache. Heparin is the first-line treatment, but in a few cases more aggressive treatments, such as local intravenous thrombolysis, mechanical thrombectomy, and decompressive hemicraniectomy, may be required.
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PMID:Cerebral venous thrombosis: an update. 1723 3

A 22-year-old male had a meniscopathy operation using spinal anesthesia. After the operation, the patient reported a throbbing headache. His brain computed tomography (CT) showed subarachnoid hemorrhage (SAH) and hyperdense dural venous sinuses suspicious for thrombosis. Filling defects were observed in the superior sagittal and right transverse sinuses on the contrast-enhanced magnetic resonance images. The patient was diagnosed with cerebral venous sinus thrombosis (CVST). On the tenth day of his admission, his clinical findings progressed and heparin therapy was initiated after resorption of hemorrhage was observed in a second non-contrast CT scan. The patient developed decreased consciousness the day after heparin administration. A subsequent brain CT revealed intraparenchymal hemorrhage in the right anteroinferior frontal region. Heparin therapy was discontinued, and anti-edema therapy was started. The presentation of CVST with SAH is a rare condition. Furthermore, development of CVST after spinal anesthesia is very rare. In this case, CVST developed after spinal anesthesia, and its first clinical presentation was SAH. To our knowledge, this is the first case CVST presenting with SAH after spinal anesthesia.
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PMID:Cerebral venous thrombosis presenting with subarachnoid hemorrhage after spinal anesthesia. 2214 Dec 92

We report a challenging case of cerebral venous sinus thrombosis (multiple etiologic factors) that was complicated by heparin resistance secondary to suspected antithrombin III (ATIII) deficiency. A 20-year-old female previously healthy and currently 8 weeks pregnant presented with worsening headaches, nausea, and decreasing Glasgow Coma Scale/Score (GCS), necessitating mechanical ventilatory support. Imaging showed extensive clots in multiple cerebral venous sinuses including the superior sagittal sinus, transverse, sigmoid, jugular veins, and the straight sinus. She was started on systemic anticoagulation and underwent mechanical clot removal and catheter-directed endovascular thrombolysis with limited success. Complicating the intensive care unit care was the development of heparin resistance, with an inability to reach the target partial thomboplastin time (PTT) of 60 to 80 seconds. At her peak heparin dose, she was receiving >35 000 units/24 h, and her PTT was subtherapeutic at <50 seconds. Deficiency of ATIII was suspected as a possible etiology of her heparin resistance. Fresh frozen plasma was administered for ATIII level repletion. Given her high thrombogenic risk and challenges with conventional anticoagulation regimens, we transitioned to argatroban for systemic anticoagulation. Heparin produces its major anticoagulant effect by inactivating thrombin and factor X through an AT-dependent mechanism. For inhibition of thrombin, heparin must bind to both the coagulation enzyme and the AT. A deficiency of AT leads to a hypercoagulable state and decreased efficacy of heparin that places patients at high risk of thromboembolism. Heparin resistance, especially in the setting of critical illness, should raise the index of suspicion for AT deficiency. Argatroban is an alternate agent for systemic anticoagulation in the setting of heparin resistance.
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PMID:Heparin Resistance and Anticoagulation Failure in a Challenging Case of Cerebral Venous Sinus Thrombosis. 2768 23


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