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

The lack of a common, widely acceptable criterion for the definition of trivial, minor, or mild head injury has led to confusion and difficulty in comparing findings in published series. This review proposes that acute head-injured patients previously described as minor, mild, or trivial are defined as "mild head injury," and that further groups are recognized and classified as "low-risk mild head injury," "medium risk mild head injury," or "high-risk mild head injury." Low-risk mild injury patients are those with a Glasgow Coma Score (GCS) of 15 and without a history of loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is definitively less than 0.1:100. These patients can be sent home with written recommendations. Medium risk mild injury patients have a GCS of 15 and one or more of the following symptoms: loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is in the range of 1-3:100. Where there is one computed tomography (CT) scanner available in an area for 100,000 people or less, a CT scan should be obtained for such patients. If CT scanning is not so readily available, adults should have a skull x-ray and, if this shows a fracture, should be moved to the "high-risk" category and undergo CT scanning. High-risk mild head injury patients are those with an admission GCS of 14 or 15, with a skull fracture and/or neurological deficits. The risk of intracranial hematoma requiring surgical evacuation is in the range 6-10:100. If a CT scan is available for 500,000 people or less, this examination must be obtained. Patients with one of the following risk factors--coagulopathy, drug or alcohol consumption, previous neurosurgical procedures, pretrauma epilepsy, or age over 60 years--are included in the high-risk group independent of the clinical presentation.
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PMID:Defining acute mild head injury in adults: a proposal based on prognostic factors, diagnosis, and management. 1149 92

Believed to be due to unbalance between cerebrospinal fluid (CSF) production rate and its loss through the spinal dural puncture hole, post-dural puncture headache (PDPH) is often considered as a physiological syndrome, usually reversible without pathological sequelae after dural hole's closure. The clinical case here presented (incapacitating headache associated with diagnostic dural puncture in a leukaemic young female patient who underwent bone marrow transplantation) shows potentially fatal pathological sequelae following prolonged headache (untreated, due to the severe postransplant immunodeficiency and coagulopathy). The observed RMI lesions suggest interesting conclusions about the clinical indications and correct timing of autologous epidural blood patch (EBP). We also suggest the ways to preventing rebound intracranial hypertension following autologous epidural blood patch in patients suffering from incapacitating and prolonged headache.
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PMID:[Severe and prolonged post-dural puncture headache: from pathological basis to therapeutic role and correct timing for epidural blood patch]. 1177 23

Gastric adenocarcinoma is rarely observed in patients under the age of 40. Meningeal carcinomatosis as a first manifestation of disease is absolutely unique. If meningeal involvement occurs it is usually secondary event in previously diagnosed tumor. The prognosis is very unfavorable associated with short term survival. In the treatment of this disease there night be used either chemotherapy administered via lumbar injection or radiotherapy or combination of both. This case study is one of very few cases reported in literature when meningeal carcinomatosis was a first sign of advanced gastric adenocarcinoma. 39 years old woman was admitted to our hospital with severe headache, diplopia and vomiting. Meningeal carcinomatosis with gastric primary was diagnosed. She was treated with combination of cytosine arabinosid (Cytosar), methotrexate (Methotrexat), hydrocortisone (Hydrocortisone) administered via intrathecal lumbar injection and whole brain radiation. As a main complication she experienced disseminated intravascular coagulopathy. The improvement of patient's condition following the initial treatment had a very limited duration and the patient died of bilateral pneumonia and cerebral edema 44th day after the admission.
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PMID:[Meningeal carcinomatosis as the first manifestation of gastric adenocarcinoma]. 1178 14

Coagulation disorders are common in cancer patients. In patients with solid tumors, a low-grade activated coagulation can result in systemic and cerebral arterial or venous thrombosis. Cancer treatments may also contribute to this coagulopathy, which usually, but not exclusively, occurs in the setting of advanced malignant disease. There may be TIAs or cerebral infarctions. Because of the widespread distribution of cerebral thromboses, there may be a superimposed encephalopathy; sometimes this is the only sign. Concurrent systemic thrombosis is present in many patients and is a useful clue to the diagnosis. In cerebral venous occlusion, the initial symptom is usually a headache. Except for cerebral intravascular coagulation that is unassociated with NBTE, neuriomaging studies usually demonstrate one or more parenchymal infarctions. MRI or MRV may demonstrate venous thrombosis. The laboratory evidence of coagulopathy is difficult to distinguish from the asymptomatic coagulopathy that often accompanies advanced cancer, and the test results must be interpreted cautiously. NBTE can be diagnosed by transesophageal echocardiography. There is no established treatment for the thrombotic coagulopathy associated with cancer, but anticoagulation should be considered. In leukemia and lymphoma, the coagulopathy is typically acute DIC that can lead to systemic and brain hemorrhages. It is especially common in acute myelogenous leukemias. The clinical signs of cerebral hemorrhage are fulminant and may be fatal. The bleeding usually occurs in the brain or subdural compartment, and rarely in the subarachnoid space. The diagnosis can be suspected by the clinical setting and by systemic thrombosis or hemorrhage. It can be established by examination of the peripheral smear, the platelet count, and tests of coagulation function. Therapy of acute DIC is controversial and should be individualized for the clinical setting. Cerebrovascular disorders can complicate metastatic or primary tumor in the brain, skull, dura, or leptomeninges. The clinical signs of infarction are indistinguishable from other causes of stroke, except that tumor-related venous occlusion will usually first produce signs of increased intracranial pressure. The diagnosis of tumor-related infarction can usually be established by neuroimaging studies that show infarction and may show extracerebral sites of tumor. CSF examination is useful in diagnosing leptomeningeal metastasis. A search for lung or cardiac tumor should be performed when embolic tumor infarction is suspected. Primary or metastatic tumors in the brain or dura may hemorrhage, producing the initial clinical signs of the brain tumor or a change in chronic signs induced by the tumor. There are helpful clues to a neoplastic hemorrhage on brain CT or MRI scans. The brain hemorrhage may require evacuation and the underlying tumor will usually require additional antineoplastic treatment. Hyperleukocytosis (extreme elevation of the cell count) in acute myelogenous leukemia is a less common cause of brain hemorrhage in recent years because of improved methods to lower the cell count. Cerebral arterial or venous thrombosis is sometimes the result of cancer therapy. The attribution of thrombosis to chemotherapy in many published cases is only speculative, because carefully conducted prospective studies that include investigation for other thrombotic causes are not available. The best-known associations with thrombosis are L-asparaginase, which is typically used in the induction therapy of acute lymphocytic leukemia, and combination hormonal therapy and chemotherapy for breast cancer. Radiation to the head and neck, typically administered for head and neck epithelial cancers or lymphoma, may result in delayed carotid atherosclerosis. The distribution of stenosis or occlusion is within the radiation portal and is typically more extensive than is atherosclerosis that develops in the absence of radiation. Small clinical series suggest that surgical treatment is equally effective as in nonirradiated carotid atherosclerosis. In children, the cerebral vessels can be affected by brain radiation resulting in stenosis or occlusion. Brain hemorrhages can result from chemotherapy effects on the hemostatic system or a microangiopathic anemia. Hemorrhages from radiation-induced vascular abnormalities are rare. Opportunistic infections, especially fungal infections, can complicate cancer or its treatment. Septic cerebral emboli may result in focal cerebral signs, seizures, or encephalopathy. Sometimes there is an associated hemorrhagic vasculitis or cerebritis. Rarely, mycotic aneurysms may bleed. A high index of suspicion is needed to diagnose fungal infection because of the difficulty in culturing the organism from the blood or CSF. A clinician can usually establish the cause of stroke in the cancer patient by performing a careful review of the clinical setting--including the type and extent of cancer and the type of antineoplastic therapy--in which the stroke occurred. Systemic thrombosis, embolism, or hemorrhage can be a clue to the cause, and appropriate neuroimaging and coagulation studies to aid in the diagnosis are available. Therapy may ameliorate symptoms or prevent further episodes. The identification of one of these unusual stroke syndromes that leads to the diagnosis of an occult and treatable cancer can be particularly rewarding.
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PMID:Cerebrovascular complications in cancer patients. 1269 Jun 49

A 31-yr-old man presented with a 1-wk history of fever, chills, weakness, headaches, and a significant 20-lb weight loss over the preceding 2 months. His past medical history was relevant for liver amebiasis during childhood. Two days before admission, the patient noticed jaundice. He denied abdominal pain or other GI symptoms, and there was no history of alcohol intake, medications, or illicit drugs. His physical examination revealed generalized jaundice, hepatosplenomegaly, and bilateral leg edema. Neurologically, the patient was agitated, with periods of disorientation, and he had bilateral flapping. His blood tests revealed pancytopenia, renal failure, liver failure, and coagulopathy. Because the patient had a fever, hepatosplenomegaly, and pancytopenia, a further workup also included a bone marrow and liver biopsy. No conclusive diagnosis could be made from the above tests, and the patient died 5 days after admission. Postmortem evaluation, including flow cytometry and gene rearrangement in the tissue obtained from the liver, revealed large B cell lymphoma. This case illustrates an unusual presentation of hepatic non-Hodgkin's lymphoma. Current information regarding this entity is scant, mainly owing to its rarity. We present a review of the literature, including the incidence, presentation, treatment, and prognosis of primary hepatic lymphoma.
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PMID:Primary hepatic non-Hodgkin's lymphomas: case report and review of the literature. 1468 34

Over a 5-year period, we investigated 77 consecutive patients (36 males, 41 females, mean age 40.9 years) referred to our hospital with the diagnosis of CNS vasculitis. Extensive workup including MRI, echocardiography, laboratory tests, angiography ( n=53), and biopsies at appropriate sites ( n=26) was performed based on individual history and symptoms. Prominent symptoms were stroke ( n=61), encephalopathy ( n=14), and headaches ( n=2). Vasculitis was finally diagnosed in 13 patients (17%) including isolated angiitis of the CNS ( n=3), giant cell arteritis ( n=4), and septic arteritis ( n=3). Thirty-two patients (42%) presented noninflammatory vasculopathies including moyamoya ( n=6), Sneddon's syndrome ( n=5), dissection ( n=4), CADASIL ( n=2), and collagen vascular disease ( n=9). Coagulopathy was found in 14 cases (18%) including antiphospholipid syndrome ( n=8) and APC resistance ( n=4). Other causes were cardiogenic embolism ( n=8), multiple sclerosis ( n=5), and migraine stroke ( n=3). Only a minority of patients referred for evaluation of suspected CNS vasculitis actually present with inflammatory vascular disease. Main differential diagnosis includes noninflammatory vasculopathies, coagulopathies, and cardiac disease. Since septic processes may be responsible for the symptoms, "blind" treatment with immunosuppressive agents should be strictly avoided.
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PMID:[Diagnosis and differential cerebral vasculitis diagnosis]. 1477 Feb 79

The reported average annual incidence of Rocky Mountain spotted fever (RMSF) in Kentucky is less than 5 per million population, although seroprevalence studies suggest that exposure to Rickettsia riskettsii, the causative agent, is relatively common among children. The experience with RMSF at Kosair Children's Hospital over a 12-year period was reviewed. Fifteen cases were identified (5 boys and 10 girls). Illness onset ranged from April to October, and 4 patients resided in Jefferson County. The classic triad of fever, rash, and headache was present in only 60% of cases, and tick attachment was reported in only 40%. On average, 6 days elapsed from onset of symptoms to initiation of appropriate antibiotic therapy. One patient suffered splenic infarction and necrosis of the digits due to shock and disseminated intravascular coagulopathy, and 2 patients died. RMSF is a significant cause of pediatric morbidity and mortality in this region of Kentucky. Affected children may reside in relatively urban parts of the state. Initial clinical features may be nonspecific. This, as well as decreased awareness of disease and (unjustified) reluctance to use doxycycline may contribute to delays in initiating therapy.
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PMID:Rocky Mountain spotted fever at Koair Children's Hospital, 1990-2002. 1515 46

A patient with a partially thrombosed fusiform giant basilar trunk aneurysm presented with devastating headache and symptoms of progressive brain stem compression. Having an aneurysm inaccessible for endovascular treatment, and after failing a vertebral artery balloon occlusion test, he was offered bypass surgery in order to exclude the aneurysm from the cerebral circulation and relieve his symptoms. A connection between the intracranial internal carotid artery and the superior cerebellar artery was created whereupon the basilar artery was ligated just distally to the aneurysm. The proximal anastomosis on the internal carotid artery was made using the excimer laser-assisted non-occlusive anastomosis (ELANA) technique, while a conventional end-to-side anastomosis was used for the distal anastomosis on the superior cerebellar artery. Intra-operative flowmetry showed a flow through the bypass of 40 ml/min after ligation of the basilar artery. An angiogram 24 hours later showed normal filling of the bypass and the vessels supplied by it, but also disclosed a subtotal occlusion of the proximal ipsilateral middle cerebral artery with delayed filling distally. The patient, who had a known thrombogenic coagulopathy, died the following day. Autopsy showed no signs of ischemia in the territories supplied by the bypass, but a thrombus in the proximal middle cerebral artery and massive acute hemorrhagic infarction with swelling in its territory and uncal herniation. Multiple fresh thrombi were found in the lungs. The ELANA anastomosis showed re-endothelialisation without thrombus formation on the inside.
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PMID:The ELANA technique: constructing a high flow bypass using a non-occlusive anastomosis on the ICA and a conventional anastomosis on the SCA in the treatment of a fusiform giant basilar trunk aneurysm. 1534 Aug 13

A 56-year-old man treated with anticoagulants complained of a gradually worsening headache. A left chronic subdural hematoma (CSH) was shown by head computed tomographic (CT) scans and the operation, one burr hole surgery under local anesthesia, itself was performed uneventfully. However, immediately after we began draining the hematoma at the patient's bedside, the patient complained of a sudden headache. CT scans showed a subarachnoid hemorrhage (SAH). Cerebral angiography was immediately performed, but the source of hemorrhage could not be found. The next day, a CT scan showed that most of the SAH had disappeared. To our knowledge, there are no previous reports of SAH of unknown origin following surgery for CSH. The likely mechanism for the occurrence of the SAH, in addition to a coagulopathy due to anticoagulant therapy, could include the possibility that the drainage of the hematoma produced a movement of the hemisphere along with hyperperfusion that resulted in the rupture of a weak subarachnoid vessel, such as a perforating artery.
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PMID:A case of unknown origin subarachnoid hemorrhage immediately following drainage for chronic subdural hematoma. 1537 34

We report a 27-year-old male who presented with headache and rapid visual impairment. He had been diagnosed with venous sinus thrombosis 3 months earlier, when he had diffuse headache, nausea and vomiting, which subsided after incomplete thrombolytic therapy. Warfarin was then prescribed without screening for coagulopathy. Ophthalmic examination revealed bilateral papilloedema, splinter hemorrhage and lipid exudates. Neuroradiological studies including magnetic resonance imaging and cerebral angiography revealed chronic partial thrombosis over superior sagittal sinus, left side transverse sinus, right side transverse and venous confluence with engorged cortical veins and secondary dural arteriovenous malformation (AVM) and reversed flow over bilateral superior orbital veins, and thrombolytic therapy was considered not feasible. Clot-assay protein S activity was decreased (25%, normal range: 65-140%). No underlying connective tissue diseases or other coagulopathies were noted. The patient's vision failed to respond to aggressive medical treatment, and he received lumboperitoneal shunt in another hospital. His vision was improved. For young patients with occlusive cerebrovascular disorder, extensive hematological investigation for coagulopathy is strongly recommended.
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PMID:Protein S deficiency associated with progressive loss of vision and intracranial venous sinus thrombosis. 1564 87


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