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

The objective of this report was to explore the clinical features of patients with cerebral infarction due to giant cell (temporal) arteritis (GCA) and its characteristic changes in pathology, and on computed tomography (CT) and magnetic resonance imaging (MRI). Three cases of cerebral infarction due to GCA, treated during the past 2 years, were analyzed. Their clinical manifestations were observed carefully, their temporal artery biopsies were performed, their immunohistochemistries were done, and CT as well as MRI were used. The results showed that all the patients had new-onset headache and temporal artery abnormality when the disease began, and there was tremor on the right limbs of 1 patient; temporal artery biopsies revealed evidence of inflammatory cell infiltration in the arterial wall, mainly including T-lymphocytes and macrophages; small cerebral infarction foci were found on CT and MRI; and the responses to corticosteroid therapies were good. The results suggest that it is important to recognize the clinical features of cerebral infarction due to GCA, including the changes of pathology and on CT and MRI. In some cases, special attention is paid to differentiating between atherosclerotic infarction and infections to avoid misdiagnosis.
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PMID:Cerebral infarction due to giant cell arteritis-three case reports. 1502 81

Carotid-cavernous fistulas (CCFs) are abnormal arteriovenous anastamoses between the carotid artery and the cavernous sinus. These fistulas may be classified by cause (spontaneous or traumatic), flow velocity (high or low), or pathogenesis (direct or indirect). The most commonly adopted classification is that described by Barrow based on arterial supply. Traumatic CCFs are almost always direct shunts between the internal carotid artery (ICA) and the cavernous sinus. General features of CCFs, which may be apparent with any lesion, including bruit, headache, loss of vision, altered mental status and neurological deficits. Some fistulae may present primarily with hemorrhage before any evaluation can be performed. However, hemiparesis has been rarely observed. Only a literature review of Murata et al reported a case of hemiparesis caused by posttraumatic CCF, in which the fistula resulted in venous hypertension and subsequent brainstem congestion. While in our case, cerebral infarction was caused by total steal of the blood flow. The patient recovered after occlusion of the fistula with a detachable balloon.
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PMID:Hemiparesis in carotid cavernous fistulas (CCFs): a case report and review of the literature. 1536 28

A 29-year-old man presented with lethargy, headache, high fever, and visual disturbance. Neurological examination showed mydriatic pupil, ptosis, diminished light reflex, and ophthalmoplegia on the left. Magnetic resonance (MR) imaging showed the typical findings of pituitary apoplexy, and cerebral angiography disclosed mild narrowing of the A1 segment of the left anterior cerebral artery (ACA). Transsphenoidal tumor resection was performed. Transient severe right hemiparesis occurred directly after the operation. Computed tomography demonstrated cerebral infarction in the territory of the left Heubner's and medial lenticulostriate arteries. Pituitary apoplexy followed by cerebral infarction is very rare. Vasospasm of the perforating arteries of the ACA probably caused the cerebral infarction. Subarachnoid blood or vasoactive agents released from the tumor were the most likely cause of the vasospasm. MR imaging findings of contrast enhancement around the vessels may indicate reactive processes around the vessels.
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PMID:Cerebral infarction following pituitary apoplexy--case report. 1560 Feb 83

We describe an 89-year-old woman who presented with an abrupt onset of headache and right hemiparesis. With the initial diagnosis of cerebral infarction, we started therapy using sodium ozagrel. The right hemiparesis worsened, however, and a continuous intravenous heparin injection showed no effect. Furthermore, nystagmus in the bilateral eyes, dysphagia, left hemiparesis, and central ventilation disorder appeared one after another in three weeks. A magnetic resonance images (MRI) of the head, performed on the fifth hospital day with regular intervals of axial sections, disclosed no lesion responsible for right hemiparesis. MRI of the brainstem and upper cervical cord, performed after two weeks with smaller intervals of axial sections, revealed a T2 high signal lesion in the left side of the medulla oblongata and upper cervical cord. After about five weeks from the onset of the disease, she died of pneumonia. With the pathological examination, we diagnosed as glioma originated in the left ventral part of medulla oblongata. Five similar cases of brainstem glioma have been reported so far. Our patient, the oldest one, showed an exceptionally rapid clinical course, instructing us to consider the possibility of medullary glioma even in the elderly patients presenting with acute onset hemiparesis followed by rapid and progressive appearance of brainstem signs.
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PMID:[An autopsied case of medullary glioma with an abrupt onset of headache and hemiparesis]. 1596 Jan 73

A thirty-two-year-old woman who had been diagnosed MELAS with 3243A > G mutation presented headache, nausea, decreased bilateral visual acuity, and topographical disturbance on January 1 in 2002. Although brain CT showed no fresh lesion, recurrence of stroke-like episode was considered. Immediately, she was treated with ubiquinone (210 mg/day, p.o.) and tocopherol nicotinate (300 mg/day, p.o.). She became confused on the fifth day. Diffusion weighted- and T2 weighted-MRI revealed appearance of hyperintense lesion at the right occipital lobe. We started edaravone infusion (30 mg, twice a day, div.) for two weeks with informed consent from her family. On 13th day her consciousness was improved. Edema and signal intensity of the lesion were decreased on MRI with minimal spread to the parietal lobe. She discharged on the 30th day with marked visual field loss, hemispatial neglect, and topographical amnesia. MRI after four months showed remarkable atrophy of the right occipital region. In our department, five stroke-like episodes including this case were treated with ubuiquinone and tocopherol nicotinate. This regimen was effective in prevention of progressive spread of lesions only in two episodes. Edaravone is radical scavenger used in acute cerebral infarction. Progressive spread into the neighboring regions is one of characteristics of MELAS, although its precise mechanisms are not well known. Oxidative stress induced by released free radicals through mitochondrial dysfunction might be one of factors and edaravone would make an effect through blockage of the free radicals. Edaravone could not rescue neurons in the initial lesion. Although more numbers of cases are needed to establish the effect of edaravone on MELAS, it could minimize the neurological deficits after stroke-like episode of MELAS.
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PMID:[A case of stroke-like episode of MELAS of which progressive spread would be prevented by edaravone]. 1602 65

A complex bidirectional relation between migraine, mostly migraine with aura (MA), and ischaemic stroke is known. A cerebral infarction can occur during a MA, and MA is a risk factor for ischaemic stroke, particularly in young women. Conversely, cerebral ischaemia can induce MA. Both ischaemic stroke and MA might be consequences of many underlying vascular disorders. Despite the relation between migraine and stroke, migraine as a primary headache disorder is mostly benign.
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PMID:Relation between migraine and stroke. 1610 60

A 56-year-old man complained of headache and the analgesia of the four extremities. Laboratory data presented signs of inflammation, but no other abnormality such as renal or respiratory dysfunction. Two months after the appearance of the primary symptoms, he developed cerebral infarction of the bilateral corona radiata. The patient did not have any of the risk factors for cerebrovascular disease. He was diagnosed with anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) because the systemic examinations revealed only that he tested positive for anti-neutrophil cytoplasmic autoantibody (ANCA). Moreover, the biopsy of the sural nerve displayed microscopic polyangitis (MPA). Despite undergoing steroid pulse therapy, the patient died from the fatal cerebral hemorrhage. The clinical course of AAV is rapid progressive. In cases of atypical cerebrovascular disease, the possibility of ANCA should be investigated.
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PMID:ANCA-associated vasculitis (AAV) causing bilateral cerebral infarction and subsequent intracerebral hemorrhage without renal and respiratory dysfunction. 1627 97

We report a case of a middle-aged man who suffered a cerebral infarction resulting from dissection of a vertebral artery associated with morning blood pressure surge. A 56-year-old man was transferred to our hospital with dizziness and vomiting in the early morning on a cold day in winter. He reported that he had been standing in front of the sink after bathing when he suddenly felt dizzy and fell down. He did not lose consciousness, and by the time he reached the hospital by ambulance, his dizziness had subsided, but he complained of severe headache and vomited 3 times. On admission, he was alert, and there were no neurological or radiological abnormalities (CT, MR angiography) in the brain. However, infarction in the left cerebellar hemisphere was detected by brain MRI on the 5th day of hospitalization. String sign of the left vertebral artery was noted by angiography, confirming the diagnosis of dissection of the left vertebral artery. Ambulatory blood pressure monitoring was performed after discharge. Although the mean 24-h blood pressure was in the normal range, a marked morning blood pressure rise was observed. We speculated that the acute rise of blood pressure in the early morning might have contributed to the dissection of the vertebral artery.
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PMID:A case of vertebral artery dissection associated with morning blood pressure surge. 1647 Nov 79

Posterior reversible encephalopathy syndrome (PRES) is a recently described variant of hypertensive encephalopathy characterized by headache, visual disturbances and altered mental function. Its causes are diverse and in contrast to hypertensive encephalopathy, it can develop without significant elevation of blood pressure. This syndrome is mostly reversible when correctly managed; however, failure to recognize it can lead to cerebral infarction and death.
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PMID:Posterior reversible encephalopathy syndrome: a variant of hypertensive encephalopathy. 1676 18

In February 2005, a 33-year-old man visited A hospital complaining of fever. The blood screening test revealed the liver dysfunction, then computed tomography showed swelling of abdominal lymph nodes. In April, headache and disorientation appeared. He was diagnosed as disseminated tuberculosis and tuberculous meningitis based on chest X-ray and computed tomography findings and examination of cerebrospinal fluid. After admission to our hospital, anti-tuberculous drugs were prescribed, but the cerebral infarction happened. The disturbance of consciousness and the left half of his body paralysis appeared. They did not improve and hydrocephalus was complicated in August, though he was treated by steroids. He needed all helps because of the left half of his body paralysis and an advanced sequelae was left. It was thought that the abdominal lymph adenopathy preceded as one of symptoms of the disseminated tuberculosis in this case. It is said to be rare that abdominal lymph node swelling is seen in the early stage of disseminated tuberculosis. But, we think that it is necessary to keep in mind that the possibility of disseminated tuberculosis as one of the diseases in differential diagnosis, when we examine enlargement of abdominal lymph nodes with symptoms suggesting the presence of infection such as fever.
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PMID:[Case of disseminated tuberculosis complicated with tuberculous meningitis while investigating an abdominal lymphadenopathy]. 1715 45


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