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

A 24-year-old woman was found comatose after 2 days of cephalalgia and vomiting. An immediate diagnosis of carbon monoxyde poisoning was disclaimed when blood carbon monoxyde was found to be 1.75 ml/100. A diagnosis of acute intracranial hypertension led to trephination with ventricular punction and brain biopsy on the third day. The patient died on the eleventh day. Ultrastructural study of biopsy tissue showed nearly normal cortex, and injured white matter, with disrupted or destroyed myelin and pycnotic oligodendroglia in contrast with nearly normal axons, astrocytes, and capillaries. Autopsy showed a typical semioval center myelinopathy. After discussion of the histotoxic, vascular, and edema theories for myelinopathy pathogenesis, primary oligodendrogial lesion is considered, and correlated with the diphasic evolution often observed in the course of carbon monoxyde myelinopathy.
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PMID:[Myelinopathy due to carbon monoxyde poisoning. A study in ultrastructural neuropathology (author's transl)]. 67 80

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

In addition to asking their patients about recent foreign travel, Canadian doctors need to be aware of what features to ask about in considering imported illnesses. Of these illnesses, malaria is one of the most common and serious. Because of its cerebral renal, pulmonary and intestinal complications, falciparum malaria must be distinguished from non-falciparum forms. Anyone with a fever who has arrived recently from an endemic area should be tested for malaria. In addition, headache, malaise, myalgias, arthralgias, low back pain, nausea, vomiting, diarrhea or cough should raise suspicion. Malaria should be remembered as a cause of coma. Persons taking any form of drug prophylaxis for malaria are not protected absolutely and those who are semi-immune can become severely ill occasionally.
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PMID:Symptoms and signs of malaria. 78 78

4 cases of thrombosis of the intracranial venous sinuses (TIVS) which occurred in patients 22-38 years of age who used oral contraceptives are discussed. Of the 29 reported cases of this type, 19 of the patients died. There are 3 stages in the evloution of TIVS: headache, hemispheric focus symptoms (e.g., Bravis-Jacksonian crises), and a phase of dramatic aggravation (e.g., severe headache, coma). Arteriography of the carotid artery and cerebral scintigraphy are the methods used to diagnose TIVS. Besides such predisposing factors as diabetes, obesity, migraines, etc., the use of oral contraceptives containing estrogen seem to be a factor in the development of TIVS, particularly within the 1st year of estrogen use. The reduction of cerebral volume seems to be the best treatment for TIVS: anticoagulants and thrombolytic compounds can cause fatal hemorrhaging
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PMID:[Thrombosis of the intracranial venous sinuses after ingestion of estroprogestative agents. 4 cases]. 88 3

A teen-age girl became comatose after the sudden onset of headache. Initial angiography did not reveal the site of bleeding. The subsequent onset of ocular bobbing directed attention to the region of the pons. Repeated angiography showed an aneurysm of the superior cerebellar artery. At surgery, the fundus of the aneurysm was adherent to the pons and there was a small hematoma within the pons. Ocular bobbing is rare, but is most commonly seen in association with destructive lesions of the pontine tegmentum, and is a useful localizing sign.
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PMID:Ocular bobbing with superior cerebellar artery aneurysm. Case report. 90 12

Since October 1967 we have performed 76 microsurgical STA--cortical MCA bypass operations. Recently we have had two cases, who died from intracerebellar hematoma following bypass operation. Intracerebellar hematoma is reported primarily due to hypertension (50-80%), and to comprise 10% of all spontaneous intracranial hematomas. Diagnosis of this lesion is frequently missed but can be made by the typical clinical picture (respiratory irregularity, pinpoint pupils, absence of oculovestibular responses, loss of consciousness), and the CT-Scan. If the correct diagnosis is made and operation promptly performed, many patients with subacute or acute intracerebellar hematoma can be saved. The 2 cases presented here had a history of hypertension and anticoagulation (including Colfarit), but had sustained the bypass operation well and showed no neurological deficit immediately after the operation. They had received Rheomacrodex intra- and postoperatively. Quite soon postoperatively, however, the systolic blood pressure rose to 210 mmHg and the patients complained of severe headache. They were treated symptomatically with analgesics and antihypertensive drugs. A short time later they became comatose and died. In order to prevent this complication after bypass surgery, postoperative management of hypertension is mandatory. The combination of antithrombic agents, Colfarit and Rheomacrodox, might have played a role in inducing the hemorrhages. Furthermore strong analgesics should be withheld to prevent their masking neurological deterioration. Intracerebellar hematoma must always be considered in hypertensive or anticoagulated patients, especially because it can be cured with prompt diagnosis and operative treatment.
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PMID:[Intracerebellar Hematoma following microsurgical STA-cortical MCA bypass surgery (author's transl)]. 90 21

Two cases of spontaneous cerebral ventriculostium are presented. The first case is that of a 3 year-old girl with a thumb-sized soft scalp tumor of the occipital region (dural hypertrophy) and hydroencephalodysplasia (Picaza). PVG revealed noncommunicating hydrocephalus with asymmetrical deformity of the lateral ventricle and agenesis of corpus callosum (Fig. 1). Ventriculoatrial shunt was performed. Three years passed under the useful life when she readmitted to our clinic complaining headache, nausea and vomiting. On the first hospital day she fell into respiratory arrest accompanied with coma after the tonic convulsion, and eventually, she died on the fourth hospital day. Postmortem examination revealed spontaneous cerebral ventriculostium which communicated with the posteromedial trigone of the left lateral ventricle (Fig. 3). Combined other malformations such as dysgenesis of the corpus callosum and only one anterior cerebral artery, etc. were found. The second case is that of a young adult, a 22 year-old male with rapidly progressing intracranial hypertension. PVG revealed marked dilatation of the lateral and the third ventricle, non-filling of the aqueduct and spontaneous cerebral ventriculostium which communicated with the posterior part of the third ventricle (Fig. 4). And insidiously he fell into akinetic mutism. After suboccipital exploratory craniotomy and ventriculo-peritoneal shunt akinetic mutism improved gradually, and he was discharged on foot after 7 months. PEG performed on June 8, 1973, showed no evidence of aqueduct obstruction and injected air passed from the fourth ventricle to the third one smoothly. He lives on now under a useful condition. These 2 cases are the first report on literatures in Japan, but presumably there must be many other cases. Since W. H. Sweet reported his own two cases of spontaneous cerebral ventriculostium on 1940, more than thirty cases have been published on literatures. However, there are found various expressions to describe the same condition (Table 1). We would like to propose that the most suitable expression is "ventriculostium" not only in deference to the originality of W. H. Sweet but also not to confuse this pathogenetic state with other similar conditions. The author's next interest is the chronological fact that from W. H. Sweet (1940) to A. Torkildsen (1948), all but one ostiums reported situated at the posteromedial trigone of the lateral ventricle, whereas after A. Torkildsen, they were found at the posterior part of the third ventricle in many cases. The reason is unknown. It would appear that three main conditions are necessary for the development of ventricluostium just beneath the tentorium. The first, there must be increased pressure within the lateral or the third ventricle. The second essential feature is the lack of any large space occupying lesion in the the infratentorial space. The third, there must be wider space between the tentorial incisura and the brain stem.
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PMID:[Spontaneous cerebral ventriculostium (author's transl)]. 94 70

A case is presented of neurilemmoma of the left oculomotor nerve occurring in a 64-year-old hypertensive woman. The incipient tumour produced ptosis, limited inwards rotation of the eyeball, and persistent pupillary dilatation on the left side. The mechanism of this process is discussed, having regard to the interruption of the fibres innervating these structures by the tumour, and considering the mode of occurrence of the ocular and pupillary impairments. The patient also had generalized athero-sclerosis and fusiform aneurysm of the terminal part of the left internal carotid artery. The symptoms of headache, seizure, coma, and temporary right hemiparesis were considered as manifestations of hypertensive encephalopathy unrelated to the tumour.
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PMID:Neurilemmoma of the oculomotor nerve. 112 61

Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & Therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.
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PMID:Management of the moribund carbon monoxide victim. 811 Mar 42

Fourteen patients developed massive putaminal-thalamic hemorrhage. All patients were young black men. They were hypertensive but without chronic hypertensive vascular changes. They had been treated with antihypertensive medication for less than 3 yr. All patients presented with a prodromal headache beginning 18-30 h before the brain hemorrhage. Initial clinical signs were heralded by a change in the headache pattern and vomiting. All patients became comatose and hemiplegic within 4-12 h. CT showed a hyperdense putaminal-thalamic hemorrhage which was 60 to 86 mm in maximal diameter. There was marked mass effect with secondary intraventricular extension. All patients died within 72 h, despite rapid and adequate blood pressure control and maximal medical treatment of cerebral edema and increased intracranial pressure.
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PMID:Massive putaminal-thalamic nontraumatic hemorrhage. 139 83


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