Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An extremely rare case of ruptured cerebral aneurysm associated with a fenestrated vertebral artery in osteogenesis imperfecta (OI) is presented. A 33-year-old female suffering from OI was admitted to our hospital with severe headache and vomiting. A CT scan revealed subarachnoid hemorrhage. Cerebral angiography with four vessel study showed a fenestration in the V3 portion of the left vertebral artery and a dilatation in its V4 portion, but no cerebral aneurysm was detected. After conservative treatment for three weeks, repeated angiography demonstrated an aneurysm of the anterior communicating artery. A neck clipping of the aneurysm was performed successfully. The patient was discharged with no neurological deficits. OI is a hereditary connective tissue disease characterized by bone fragility. From her family history and clinical findings, the patient was suspected to have OI type I of Sillence's classification. Among the connective tissue diseases, OI does not have complications in the cerebrovascular system as frequently as other connective tissue diseases do, for example, Marfan's syndrome, Ehlers-Danlos syndrome, or pseudoxanthoma elasticum. Carotid-cavernous fistula and moyamoya disease have been the only complications reported in OI. However, dilatation of the aortic root and increased vascular fragility have been reported recently in OI. Although this is the first reported case of a ruptured aneurysm accompanied by a fenestration and a dilatation of the vertebral artery associated with OI, it was suggested that vascular fragility caused by collagen abnormality might affect the cerebral vasculature.
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PMID:[A case of ruptured cerebral aneurysm associated with fenestrated vertebral artery in osteogenesis imperfecta]. 775 27

The nucleus caudatus is not a common location of spontaneous intracerebral hemorrhage. Twelve patients (8 men and 4 women) aged 38-76 years who had caudate hemorrhage between November 1, 1992 and March 31, 1994 were evaluated. These cases represented 2.1% of intracerebral hemorrhage cases at Neurological Institute, Veterans General Hospital-Taipei, Taiwan. Cerebral angiography was performed on eight patients. Six patients were evaluated by an extensive neuropsychological battery. The most frequent symptoms of caudate hemorrhage were headache and/or vomiting, and decreased consciousness. Clinical features were similar to those of subarachnoid hemorrhage. Angiography showed characteristic moyamoya disease in one patient but did not show an aneurysm or arteriovenous malformation in any patient. The etiology in most patients was hypertension. Neuropsychological assessments showed significant impairment in tasks of short-term and long-term memory and in verbal fluency as well as trends of impairment of orientation rather than of controls. Neurobehavioral symptoms probably resulted from interruption of the cortical-subcortical loops between the caudate nucleus and prefrontal cortex.
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PMID:Caudate hemorrhage: clinical features, neuropsychological assessments and radiological findings. 859 95

A 19-year-old male presented with intraventricular hemorrhage manifesting as sudden onset of headache. Angiography showed mild stenotic changes in the distal internal carotid artery and proximal anterior cerebral artery only on the right. The anterior choroidal artery and lenticulostriate arteries appeared dilated, and an aneurysm-like shadow was seen in the distal right anterior choroidal artery. He was discharged without treatment. Eighteen months later, he presented with a second intraventricular hemorrhage manifesting as sudden occipitalgia, vomiting, and nausea. He had hyperreflexia of the left extremities and paresthesia of the left upper extremity. Angiography showed marked progression of the vascular abnormalities bilaterally. Moyamoya vessels were also present. He received bilateral encephalo-duro-arterio-myo-synangiosis with good results. Moyamoya disease may cause hemorrhage even at an early stage.
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PMID:Ventricular hemorrhage at an early stage of moyamoya disease--case report. 905 43

A 59-year-old woman suffered from sudden onset of severe headache and vomiting for five days, with normal consciousness. A computerized tomography (CT) scan showed acute subdural hematomas in the right frontal and left frontotemporoparietal regions. As there was no history of head injury, the patient underwent bilateral carotid angiography. The left carotid angiogram showed total occlusion of the left middle cerebral and anterior cerebral arteries with a moyamoya pattern of collateral circulation. Five days later, the patient suddenly lost consciousness associated with right hemiparesis. An emergency CT scan disclosed diffuse acute brain tissue edema in the left cerebral hemisphere with uncal/transtentorial herniation, caused by acute infarction in the territory of the left middle cerebral artery. The patient died 10 hours later. The acute infarction was considered to have been caused by subdural hematomas compressing the transdural anastomoses, thus eliminating all blood supply to the region of the left middle cerebral artery.
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PMID:Moyamoya disease causes acute subdural hematomas and sudden death: a case report. 983 Feb 41

Intracranial aneurysms associated with moyamoya disease are often reviewed. Aneurysms not around the circle of Willis but on the collateral vessels are rare. A 71-year-old woman presented with sudden onset of severe headache and vomiting. CT scan showed an intraventricular hemorrhage from bilateral lateral ventricle to fourth ventricle. Cerebral angiography showed the occlusion of the terminal portion of the bilateral internal carotid artery with moyamoya vessels and three aneurysms at the distal portion of the left lateral posterior choroidal artery. Clinical symptoms improved day by day, but 17 days later, due to rebleeding of the aneurysms the patient fell into coma. The day after rebleeding, endovascular embolization was performed using liquid particle, and the left lateral posterior choroidal artery and the aneurysm were occluded. Brain infarction with massive brain edema of the left cerebral hemisphere resulted in the patient's death. The management of the aneurysms in the basal ganglia and on the collateral vessels associated with moyamoya disease is controversial. We suggest positive intervention during the acute stage for the peripheral artery aneurysms taking endovascular embolization into consideration to prevent rupture or rebleeding.
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PMID:[Moyamoya disease with intraventricular hemorrhage due to rupture of lateral posterior choroidal artery aneurysm: case report]. 1056 52

A 29-year-old male with Down's syndrome presented with severe headache and vomiting. Computed tomography demonstrated subarachnoid hemorrhage. Left carotid angiography showed severe stenosis of the middle cerebral artery 2 cm distal to its origin, as well as abnormal hyper-vascularization near the stenosis site similar to that seen in moyamoya disease. Right carotid angiography showed no abnormalities. However, slight stenosis of the distal part of the bilateral vertebral arteries was noted. There was no aneurysm. We judged that the subarachnoid hemorrhage had been caused by rupture of the moyamoya-like vessel. Some patients with Down's syndrome have anatomical vascular abnormality and vascular fragility. The cerebral vascular abnormality found in this case may be part of the systemic vascular abnormalities associated with Down's syndrome. The vascular changes in some adult patients with Down's syndrome may be a sign of premature aging, and long-term studies with periodic vascular examination of patients with Down's syndrome need to be performed.
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PMID:Unilateral middle cerebral artery stenosis in an adult with Down's syndrome--case report. 1085 21

A 4-year-old girl was admitted to our department with the complaints of severe headache, nausea, vomiting, and photophobia. She had a 1-year history of migrainelike headache that occurred every 1 to 2 months. Her neurologic examination was normal, but T-weighted axial magnetic resonance imaging (MRI) of the brain showed flow void within the basal ganglia owing to parenchymal vascular collaterals. Magnetic resonance angiography and digital substraction carotid angiography showed both occlusion of the internal carotid artery in the supraclinoid portion and extensive parenchymal vascular collaterals. Because there was no evidence of risk factors for cerebral arterial occlusion and cerebral infarct or hemorrhage, she was diagnosed as having moyamoya disease. In any case of atypical migrainelike headache, a detailed investigation should be kept in mind to detect an underlying vascular disease such as moyamoya.
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PMID:Moyamoya disease presented with migrainelike headache in a 4-year-old girl. 1282 23

A case with arteriovenous malformation (AVM) associated with moyamoya phenomenon is reported. The 44 year-old female patient was presented with headache and vomiting. Computed tomography (CT) scan showed intraventricular hemorrhage. Cerebral angiography showed right frontal AVM and severe stenosis of right internal carotid artery. The AVM was fed by typical moyamoya vessels, Heubner's artery, and external carotid artery (ECA). We tried to embolize a bleeding point, compartment attached to lateral ventricle, but we could not. So, we embolized feeders from ECA and sent the patient to radiosurgery. We discuss here treatment and etiology of such rare condition.
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PMID:[A case of arteriovenous malformation associated with moyamoya phenomenon]. 1514 5

A female, 2 years and 7 months of age, was admitted to the hospital with stupor and nystagmus following projectile vomiting. She had been prenatally diagnosed with trisomy 12p with a familial pericentric inversion of chromosome 12 originating from her mother. She manifested developmental delay and some dysmorphic features of the face and limbs compatible with the clinical features of trisomy 12p. Four-vessel cerebral angiography revealed severe stenosis and occlusion of the supraclinoid portion of the right and left internal carotid arteries with numerous collateral vessels in the vicinity of the occlusion. These features are consistent with moyamoya syndrome. This report presents the first case of moyamoya syndrome with trisomy 12p with a familial pericentric inversion of chromosome 12.
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PMID:Moyamoya syndrome in a child with trisomy 12p syndrome. 1713 18

MELAS (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) is a maternally inherited disorder characterized by recurrent cerebral infarctions that do not conform to discreet vascular territories. Here we report on a patient who presented at 7 years of age with loss of consciousness and severe metabolic acidosis following vomiting and dehydration. She developed progressive sensorineural hearing loss, myopathy, ptosis, short stature, and mild developmental delays after normal early development. Biochemical testing identified metabolites characteristic of medium-chain acyl-CoA dehydrogenase (MCAD) deficiency (hexanoylglycine and suberylglycine), but also severe lactic acidemia (10-25 mM) and, in urine, excess of lactic acid, intermediates of the citric cycle, and marked ketonuria, suggesting mitochondrial dysfunction. She progressed rapidly to develop temporary cortical blindness. Brain imaging indicated generalized atrophy, more marked on the left side, in addition to white matter alterations consistent with a mitochondrial disorder. Magnetic resonance angiography indicated occlusion of the left cerebral artery with development of collateral circulation (Moyamoya syndrome). This process worsened over time to involve the other side of the brain. A muscle biopsy indicated the presence of numerous ragged red fibers. Molecular testing confirmed compound heterozygosity for the common mutation in the MCAD gene (985A>G) and a second pathogenic mutation (233T>C). MtDNA testing indicated that the muscle was almost homoplasmic for the 3243A>T mutation in tRNALeu, with a lower mutant load (about 50% heteroplasmy) in blood and skin fibroblasts. These results indicate that mitochondrial disorders may be associated with severe vascular disease resulting in Moyamoya syndrome. The contribution of the concomitant MCAD deficiency to the development of the phenotype in this case is unclear.
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PMID:Progressive cerebral vascular degeneration with mitochondrial encephalopathy. 1820 88


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