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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic dural arteriovenous malformation which occurs in the posterior fossa uses predominantly transverse and sigmoid sinuses. Cavernous sinus comes next and others are rather rare. However, we have recently experienced such a rare case which was operated on and cured completely. The malformation was fed through the anterior ethmoid artery and drained to the cortical vein. The case was a 36-year-old male and admitted in our clinic for having headache and nausea as the chief complaints. He was diagnosed subarachnoid hemorrhage due to the following findings: CT scans showed a high density zone localized in the sylvian vallecula. Cerebrospinal fluid obtained by a lumbar puncture was found to be bloody. No neurological abnormality other than neck stiffness and positive Kernig's sign was observed. Under study of right carotid arteriography, dural AVM was evident. The anterior ethmoidal artery which branched out from the ophthalmic artery fed the AVM. The cortical vein which ran on the surface of the frontal base was its drainer via a small nidus. There was no abnormality seen on a left carotid arteriogram. Surgery was proceeded with the right frontal craniectomy in extra- and intradural approach. At first, anterior ethmoidal artery was cut at the cribriform plate extradurally. After dura was incised, both the nidus and drainer were coagulated intradurally. The nidus was located at inner surface of the dura. The arachnoid hemorrhage was thought to be caused by rupture of this drainer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dural arteriovenous malformation of the anterior fossa with subarachnoid hemorrhage]. 380 1

This 74-year-old female suddenly complained of severe headache, nausea, vomiting and dizziness on June 19, 1981. She was brought to nearby hospital. During the following six days, the state of consciousness gradually worsened and left-sided hemiparesis and convulsion attack arose and she was admitted to our clinic on June 25, 1981. Cerebral angiograms revealed an aneurysm of the right middle cerebral artery. Diagnosis of subarachnoid hemorrhage due to the rupture of an aneurysm was tentatively made and conservative therapy was done. On the second hospital day, she had nasal bleeding and began to excrete tar-like stool. Laboratory examination revealed thrombocytopenia, increase of FDP and prolongation of prothrombin time. Her liver and renal functions gradually worsened after this episode. On the 13th hospital day, she expired. General autopsy showed wide spread adenocarcinoma with metastases to the lung, lymph nodes and bones. Examination of the head revealed an unruptured aneurysm and bilateral diffuse subdural clotted hemorrhage. The dura was tightly adherent to the skull and partially thickened. No abnormal findings were found in the brain. On microscopical examination of the dura, there were fresh hemorrhage and many of the innumerable dilated small vessels contained tumor in the inner dural layer. Even by extensive examination, the origin of the malignancy could not be identified. We concluded that the initial symptoms just like of subarachnoid hemorrhage were due to the dural metastasis and subdural hematoma. Sixteen cases of subdural hematoma secondary to metastatic neoplasm were reported previously. We made some discussion about the pathogenesis and symptomatology of this type of subdural hematoma.
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PMID:[Subdural hematoma due to metastatic dural carcinomatosis associated with DIC--a case report]. 662 89

The occurrence of hemorrhage from pituitary adenoma (so-called "pituitary apoplexy") was investigated in a consecutive series of 560 cases operated on during the past 30 years. There were 93 cases (16.6%) in which hemorrhage from pituitary adenomas was confirmed either clinically or surgically. These patients were analyzed in terms of age, sex, symptoms and signs, size of tumor, hormonal function, and histological types of adenomas, and computerized tomography findings. In 90 cases (16.6%), hematoma or old bloody fluid was verified within the tumor tissue at surgery. Three other patients presented with subarachnoid hemorrhage, but there was no detectable intratumor hematoma in any of them. Among these 93 patients, 42 (7.5%) showed no evidence of clinical symptoms related to hemorrhage (asymptomatic hemorrhage). Fifty-one patients (9.1%) had definite histories of an acute episode that suggested sudden bleeding (symptomatic hemorrhage: pituitary apoplexy). Thirty-eight patients (6.8%) had a major attack manifested by disturbances of consciousness, hemiparesis, loss of vision, or ocular palsy. In two acromegalic patients, pituitary apoplexy developed during bromocriptine treatment. There was one case of sudden death due to massive hemorrhage from the tumor 14 months after the completion of postoperative radiation therapy. The other 13 symptomatic patients (2.3%) developed a minor attack which included headache, nausea, vomiting, and vertigo. Bleeding from pituitary adenomas was not statistically correlated with any of the following factors: sex, hormonal function of adenomas, and histological types, but it was correlated with age. The number of asymptomatic cases in the third decade was significantly greater than that of the whole group of pituitary adenoma patients in the same decade. The present investigation revealed that the incidence of pituitary apoplexy was unexpectedly high: a major attack in 6.8% of pituitary adenoma patients, a minor attack in 2.3%, and asymptomatic hemorrhage in 7.5% of the cases. This risk of pituitary apoplexy should be kept in mind in treating pituitary adenomas.
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PMID:Pituitary apoplexy: its incidence and clinical significance. 725 41

We present a case of a sixteen year old boy with coarctation of the aorta who suffered ruptured cerebral aneurysm. Both cerebral and aortic lesions were successfully corrected. He complained of sudden headache and nausea. Subarachnoid hemorrhage was diagnosed by computed tomography of the head. Cerebroangiography demonstrated coarctation of the aorta. Clipping of cerebral aneurysm was done at first, then three months later, complete resection of the aortic coarctation and artificial graft replacement was done by using femoral veno-arterial cardiopulmonary bypass.
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PMID:[A case of successful surgical treatment for coarctation of the aorta associated with ruptured cerebral aneurysm]. 786 Oct 67

A 42-year-old woman suddenly developed headache and nausea on July 26, 1991, and the computed tomography (CT) scan showed a moderate-sized hematoma in the left occipital lobe. After one month's conservative treatment, she had recovered to a neurologically intact state. Cerebral angiography demonstrated a giant arteriovenous malformation fed by enlarged branches of the left posterior cerebral artery as well as small branches arising from the middle cerebral artery, anterior cerebral artery and the meningeal branches of the middle meningeal artery and the occipital artery. Preoperative embolization was planned on February 24, 1992. During an attempt at catheterization of the basilar artery and the left posterior cerebral artery with a balloon catheter and a Tracker-18 catheter, the patient complained of an intensification of her headache, nausea and vomiting. So the embolization procedure was stopped. The CT scan taken immediately at that time showed a severe subarachnoid hemorrhage (SAH). She became comatose about 40 minutes later. CT scan taken next day revealed also a complication of the pontine hemorrhage. Neurologically, she had gradually recovered and could communicate with some simple words 3 months after SAH. The total removal of the AVM was performed on May 26, 1992. Postoperative course was uneventful. She showed rapid and remarkable improvement in her neurological state suggesting that the blood flow in the surrounding brain area had been corrected. A blood deficit had no doubt been caused when blood had been stolen by the giant AVM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Subarachnoid hemorrhage and pontine hemorrhage followed by an embolization procedure of left occipital giant arteriovenous malformation: a case report]. 841 9

A retrospective analysis of all patients admitted with the diagnostic codes of aseptic or viral meningitis was performed at two institutions over 3 years. Forty-one patients with cerebrospinal fluid confirmation of aseptic meningitis (increased protein; increased white count; negative gram stain; and negative fungal, tuberculosis, and bacterial cultures) were analyzed. All the patients had headache, which was typically severe and bilateral in 39 of the 41 patients. The headache was of abrupt onset or the worst of the patient's life in 24 of the patients. The quality of the headache, when described, was usually throbbing (11 of 14). Nineteen patients had prodromal symptoms, including malaise, myalgia, gastrointestinal symptoms, and urinary tract infections. All had associated symptoms, including nausea (25), vomiting (23), photophobia (18), stiff neck (25), and back pain (11). Thirty patients were febrile. Lumbar puncture was performed for headache and fever unexplained by systemic illness in 30 patients, meningeal signs in 15, headache of abrupt onset or the worst headache ever in 24, neurologic signs or symptoms in 12, and for other reasons in 2. Computerized tomography, when performed, was negative in all cases. Focal neurologic findings were present in 5 patients, a decreased level of consciousness in 6, and papilledema in 1. A severe headache that worsens, is abrupt in onset, or is the worst of the patient's life could be due to aseptic meningitis, bacterial meningitis, or a subarachnoid hemorrhage. Although not universally present, meningeal signs, fever, and neurologic signs or symptoms should alert one to a possible central nervous system infection.
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PMID:Headache associated with aseptic meningitis. 853 Feb 75

Computed tomography (CT) findings of chronic subdural hematomas are usually diagnostic, unless hematomas are isodense and bilateral. The authors report two cases of bilateral chronic subdural hematomas, in which CT scans on admission were both misdiagnosed as delayed subarachnoid hemorrhage (SAH). The first case was a 43-year-old woman who suffered from a sudden onset of headache and nausea. She had no past history of head injury. CT scans on admission did not clearly reveal the Sylvian fissures and the mesencephalic cistern, without any mass effects. A lumbar puncture demonstrated xanthochromic cerebrospinal fluid (CSF), which was considered to be responsible for her headache. Cerebral angiography performed on day 4 failed to demonstrate any cerebral vascular disorders. Follow-up CT scans on day 7 demonstrated a high density lesion in the left subdural space. Magnetic resonance images (MRIs) confirmed a diagnosis of bilateral chronic subdural hematomas. Removal of the hematomas cleared all signs and symptoms smoothly. The second case was a 44-year-old man who was referred from another hospital because of xanthochromic CSF found by lumbar puncture. He began to suffer headache and be subject to vomiting 6 weeks earlier and these symptoms were still present on the day of admission. CT scans did not clearly show the cerebral cisterns without mass effects. Because the second lumbar puncture showed xanthochromic CSF again, SAH from aneurysm was suspected. However, emergency cerebral angiography failed to demonstrate cerebral aneurysms. MRI performed two days later demonstrated bilateral chronic subdural hematomas. Following surgery, the patient improved immediately and was discharged from hospital without any complications. In both cases, a retrospective study of the angiograms revealed the evidence of bilateral avascular areas over the convexities in the venous phase. The reason why these subdural hematomas were missed at the time of angiography was due to too much attention being paid to the arterial phase in an effort aimed only at identifying cerebral aneurysms. There are no reports of chronic subdural hematoma which demonstrated sudden onset of headache associated with xanthochromic CSF.
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PMID:[Bilateral chronic subdural hematomas presented with subarachnoid hemorrhage: report of two cases]. 867 8

A case is presented of a de novo aneurysm of the distal posterior inferior cerebellar artery with intraventricular hemorrhage. A 67-year-old woman was admitted to our hospital with sudden onset of severe headache and loss of consciousness. Computed tomography (CT) scans showed subarachnoid hemorrhage. Angiography demonstrated three aneurysms: an aneurysm of the right vertebral-posterior inferior cerebellar artery, an aneurysm of the bifurcation of the basilar artery, and an aneurysm of the left middle cerebral artery. Considering the distribution of the hemorrhage on CT scans, we concluded that the cause of the hemorrhage was rupture of the vertebral-posterior inferior cerebellar aneurysm. The vertebral-posterior inferior cerebellar aneurysm and the middle cerebral aneurysm were successfully clipped, postoperative angiograms showing the complete clippings. At that time, however, there were no abnormal findings in the left posterior inferior cerebellar artery. Six years later, she was readmitted to our hospital because of sudden onset of headache, nausea, and vertigo. CT scans showed an intraventricular hemorrhage, especially in the fourth ventricle, although subarachnoid hemorrhage was not clearly found. Angiography revealed an aneurysm of the left distal posterior inferior cerebellar artery. She underwent clipping of the aneurysm verified by postoperative angiograms. However she had bacterial meningitis and died from pneumonia and disseminated intravascular coagulopathy. De novo aneurysms of the anterior circulation have often been reported. Carotid, ligation, smoking, the use of oral contraceptives, congenital anomalies and hypertension are major risk factors in the formation of aneurysms. A de novo aneurysm of the distal posterior inferior cerebellar artery is, however, extremely rare. In this case, the right posterior inferior cerebellar artery disappeared when the de novo aneurysm was found. So it is supposed that hemodynamic changes caused by the clipping of the right vertebral-posterior inferior cerebellar aneurysm and the left middle cerebral aneurysm had contributed to the formation of the de novo aneurysm of the left distal posterior inferior cerebellar artery. In the present study, we review the literature on the aneurysm at the distal posterior inferior cerebellar artery and on the de novo aneurysm of the vertebrobasilar artery, and discuss the radiological findings and features.
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PMID:[A case of de novo aneurysm of the distal posterior inferior cerebellar artery with intraventricular hemorrhage]. 869 75

A case of Iotrolan encephalopathy is reported. A 66-year-old woman, suffering from subarachnoid hemorrhage, was admitted to our department on January 17th, 1995. After an operation for aneurysmal clipping and ventriculo-peritoneal shunt, she was discharged with no neurological deficiency. CT scan revealed ventricular enlargement and slight periventricular lucency. She was re-admitted on January 4th, 1996. She was suffering from nausea, vomiting, right hemiparesis, right hemi-hypesthesia and disturbance of consciousness. CT scan demonstrated right thalamic bleeding and bilateral ventricular hemorrhage. Further ventricular enlargement was also revealed. With medical treatment, her symptoms were relieved gradually. But disorientation and memory disturbance continued. Shuntography with Iotrolan was performed on February 2nd, 1996. The ventriculo-peritoneal shunt was demonstrated to be occluded on the abdominal side. The volume of Iotrolan used was about 8cc. She became very restless on the night of the examination. Her temperature was up to 38. CT on February 4th demonstrated brain penetration of the Iotrolan. Revision of ventriculo-peritoneal shunt, administration of steroids and hydration was performed. CSF findings demonstrated no abnormalities. Her symptoms were relieved gradually. Iotrolan is a non-ionic contrast media of dimer type, composed of C37 H48 I6 N6 O18. Its distinctive features are low distributing coefficient and high affinity with water. Contrasting several reports of Metrizamide encephalopathy, only 2 cases of Iotrolan encephalopathy were reported. Iotrolan is reported to be much safer than Metrizamide. We were able to find brain penetration by Iotrolan. It is expected to be a characteristic radiological finding of encephalopathy induced by contrast media. The mechanism of Iotrolan encephalopathy is obscure. Several theories concerning Metrizamide encephalopathy are proposed. These are (1) inhibition of hexokinase, (2) inhibition of acethylcholinesterase, (3) immunological mechanism and (4) vascular disturbance. Iotrolan has no 2-deoxy-glucose structure. The inhibition theory of hexokinase is least expected. Related matters are circulatory disturbance of liquor, dehydration, excessive contrast media, advanced age, diabetes mellitus, hypertension, epileptic patients and patients taking phenothiazines. Prompt therapy is important. Removal of contrast media, hydration and administration of steroids should be performed as early as possible.
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PMID:[A case of Iotrolan encephalopathy]. 893 76

Headache is a common complaint in emergency departments, but only a small percentage of patients have a serious disease. Nevertheless, some forms of headache, such as "warning headaches", need special attention. By far the most common symptom associated with aneurysmal minor bleed (warning leak) is a sudden headache that is considered to be a warning symptom of impending aneurysmal rupture. In the presence of sudden severe headache with or without meningeal signs or nausea, subarachnoid hemorrhage should always be considered. Recognition of these warning headaches probably offers the best opportunity of reducing the otherwise serious mortality and morbidity of aneurysmal subarachnoid hemorrhage. This report describes 7 non-consecutive patients presenting warning headaches before major aneurysm rupture. Based on our experience and a review of the literature, we recommend a management algorithm for patients presenting with sudden severe headache.
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PMID:[Sentinel headache: a premonitory symptom too often unrecognized in intracranial ruptured aneurysm]. 919 93


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