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)

We examined potential clinical and pathologic correlates of seizures among the 3,291 children in the Childhood Brain Tumor Consortium database. Fourteen percent had seizures prior to their hospitalization for a brain tumor. Among children who had a supratentorial tumor, seizures occurred in 22% of those less than 14 years of age. The prevalence of seizures increased to 68% of older teenagers. Among children with an infratentorial tumor, the prevalence of seizures was relatively constant at 6% over all age groups. The onset of seizures began more than one year prior to surgical tumor removal in over half of the children aged five or more with supratentorial tumors, significantly longer than for those of the same age with infratentorial tumors. Almost all children (98.9%) with an infratentorial tumor and seizures had at least one other symptom and more than three-fourths of them had at least three. Eighty-nine percent of children with a supratentorial tumor and seizures had at least one other symptom and more than one-half had at least three symptoms. Regardless of whether the tumor was above or below the tentorium, confusion or stupor and coma were more common in children with seizures than in children without seizures. Among children with supratentorial tumors, symptoms of a declining academic performance or an abnormality of personality, speech, walking, or sensation were significantly more frequent in children with seizures, while visual symptoms (other than visual loss or diplopia) and nausea or vomiting were less frequent. Among children with supratentorial tumors, those who had seizures were more likely to have paralysis of an arm, hand, or face, confusion or stupor, or coma and less likely to exhibit irritability, papilledema, optic atrophy, decreased visual acuity, pupillary abnormalities, or abducens paresis. Among children with infratentorial tumors, those with seizures were significantly less likely to have truncal ataxia, but more likely to experience confusion, stupor, or coma. In the supratentorial compartment, astrocytoma (nos), protoplasmic astrocytoma, anaplastic astrocytoma, and ependymoma were more frequently associated with seizures than was craniopharyngioma. No infratentorial tumor type was more or less likely to be associated with seizures. All common tumor types that were represented in both the supratentorial and the infratentorial compartment except astrocytoma (nos) were associated with significantly greater rates of seizures when located in the supratentorial compartment. The tumor location with the highest incidence of seizures was, as expected, the superficial cerebrum. More than 40% of the children with such tumors had seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of seizures in children with brain tumors. The Childhood Brain Tumor Consortium. 154 79

In this report we present aspects of the epidemiology of headache (i.e., pain in the head, face, ear, or neck) among children with brain tumors. The data are derived from the 3,291 subjects in the Childhood Brain Tumor Consortium databank. Overall, 62% of the children with brain tumors experienced chronic or frequent headaches prior to their first hospitalization: 58% of children with supratentorial tumors and 70% of children with infratentorial tumors. The relative frequency of headache increased through age 7 and then leveled off regardless of tumor location. For children under age 5, headache rarely had a duration of more than 1 year prior to hospitalization. Among children over age 4, headache duration of at least one year was significantly greater for supratentorial than for infratentorial tumors. Children with a brain tumor and headache had a different distribution of symptoms and neurologic signs than those without headache. Tumor location and headache status were interactively associated with the presence of other symptoms and neurologic signs. Children with headache had a greater number of other symptoms and neurologic signs. Regardless of tumor location among children with headache, nausea or vomiting, papilledema, and hypoactive tendon reflexes were more frequent, while upper extremity weakness, optic atrophy, and irritability were less frequent. Diplopia, coma, stiff neck, anesthesia or hypesthesia, pupillary abnormalities, and abnormalities of personality, academic performance, or speech were associated with headache in children with supratentorial tumors. No specific symptoms or neurologic signs were associated with headache in children with infratentorial tumors. Supratentorial craniopharyngioma, ependymoma, and protoplasmic astrocytoma were associated with significantly high rates of headache as was infratentorial pilocytic astrocytoma.
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PMID:The epidemiology of headache among children with brain tumor. Headache in children with brain tumors. The Childhood Brain Tumor Consortium. 202 72

A 19-year old woman who developed rapid nausea, vomiting, tachypnea, and alkalosis within 90 min of taking 3.25 g quinine S04 to induce abortion, was found to have an elevated anion gap and other electrolyte abnormalities. She was normovolemic, and had benign findings on drug screen except for quinine. Her abnormal laboratory values were high serum anion gap of 20 (normal 8-14), high urine anion gap of 171, low HC03- of 29 mEq/L, high Pa)@ of 130 mm Hg, alkalotic pH of 7.5, and hypokalemia of 2.6 mEq/L. Her hypokalemia was judged due to diuresis and vomiting. She was successfully treated with intravenous fluids and supportive care and was discharged on the third day. Quinine intoxication can also cause cinchonism, which is marked by tinnitus, vertigo, blurred vision and scotomata, and possible optic atrophy or death. The toxic dose is 2 g, and the lethal dose 8 g.
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PMID:Self-induced abortion and an elevated anion gap. 249 93

We report a 9 year-old boy with MELAS. High dosed oral thiamine administration and high fat diet induced remarkable neurological and biochemical improvement. His mother had episodic headaches and hemiplegia, probably MELAS. He complained muscle weakness and repeated episodes of vomiting started from 2 years of age. High levels of serum lactate and pyruvate were recognized, but with no metabolic acidosis. He developed generalized muscle weakness, growth retardation, generalized convulsions and stroke-like episodes at 5 years old. Optic nerve atrophy and mental retardation gradually appeared. A muscle biopsy at 5 years old revealed numerous ragged-red fibers with excess accumulation of lipid droplets and glycogen particles. Scattered fibers had no cytochrome c oxidase (CCO) activity representing focal CCO deficiency. An electron microscopy showed markedly increased number of giant mitochondria filled with markedly proliferated complicated cristae. Pyruvate dehydrogenase complex level in the fibroblasts was within normal ranges. Serum carnitine level was normal. With oral administration of thiamine hydrochloride (1000 mg) and high fat diet (60-70%), muscle weakness improved, and lactate and pyruvate levels in the serum reduced to normal ranges, whereas the mental deterioration, muscle atrophy, pes cavus progressed very slowly. He died from cardiac and renal failures at 9 years old. Autopsied muscles showed a marked decrease in cytochrome c oxidase activity (biochemically 12.8% of the normal level), and almost all muscle fibers had no cytochrome c oxidase activity histochemically. The progression of the MELAS was probably in parallel with the decrease in CCO activity.
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PMID:[A case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) with progressive cytochrome c oxidase deficiency]. 255 13

A 12-year-old boy with corticosteroid-responsive mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is described. His mother proved to have an asymptomatic mitochondrial myopathy on examination of a muscle biopsy specimen. Three weeks after the onset of vomiting, headache, ataxia and visual and speech impairment, he presented with a background of somatic growth retardation, deafness and school failure. Examination revealed disorientation, dysphasia, dyspraxia, optic atrophy, hemianopia, hemiparesis and sensory inattention. A cranial computed tomographic scan disclosed a large, low-density area, which was consistent with infarction, in the left posterior hemisphere and marked calcification of the basal ganglia bilaterally. Within two weeks of the commencement of corticosteroid treatment, the neurological dysfunction resolved. Attempts to decrease the dosage of dexamethasone caused an exacerbation of symptoms repeatedly. Two weeks after ceasing corticosteroid therapy, the patient developed a serious neurological relapse and a new, large, low-density area, which resembled an infarction, in the right posterior hemisphere on a computed tomographic scan. The reintroduction of corticosteroid therapy again resulted in the rapid resolution of all symptoms. It became evident that the patient had an exquisitely sensitive corticosteroid dependency, whereby a reduction in the dexamethasone dosage of even 0.25 mg a day caused confusion, headaches and increasing lactic acidaemia. Although it is difficult to assess the impact of various therapies in MELAS because of the episodic natural course of the disease, this remarkable corticosteroid responsiveness also has been noted in four previously reported patients with MELAS syndrome; therefore, it would seem reasonable to suggest that corticosteroid therapy now should be considered as standard treatment for this condition. However, corticosteroid therapy in other forms of mitochondrial disorders still awaits careful evaluation.
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PMID:Mitochondrial encephalomyopathy with corticosteroid dependence. 273 98

A 55-year-old man with a subacute onset of slurred speech, ataxia, nystagmus, extrapyramidal rigidity, decreased tendon reflexes, vomiting, bilateral optic atrophy, and clonic jerks died of bronchopneumonia and respiratory failure. Neuropathological examination showed lesions characteristic of subacute necrotizing encephalopathy. Clinicopathological observations of reported cases of Leigh's syndrome in the adult are reviewed.
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PMID:Leigh's syndrome in an adult. 652 Jun 17

Brain involvement in hydatid disease occurs in 1 to 2% of all Echinococcus granulosus infections. Fifty to 75% of intracranial hydatid cysts are seen in children. This study included 19 children who underwent surgery for intracranial hydatid cysts between January 1979 and September 1992. There were 12 boys and 7 girls, ages 3 to 16 years (mean, 8.1 yr). Headache and vomiting were the predominant symptoms. Papilledema was present in 16 patients, and 2 patients had secondary optic atrophy. A round, cystic lesion without perifocal edema and rim enhancement was detected on the computed tomographic scans of 13 patients. The cystic lesions with rim enhancement and perifocal edema were noted on the computed tomographic scans of 3 patients. Of these three patients, two subsequently had a recurrence. Total removal of the cyst without rupture was achieved in 12 patients. Only a 3-year-old boy in whom the cyst ruptured at surgery died. Seven patients in whom either the hydatid cyst ruptured at surgery or there was systemic hydatid disease received mebendazole therapy. Mebendazole seems to be effective in hydatid disease. Cerebral hydatid cysts should be removed in toto without rupture. The preoperative diagnosis is very important in planning surgery. When a cystic lesion is detected on computed tomographic scan, hydatid disease should be taken into consideration in countries where hydatid disease is endemic.
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PMID:Intracranial hydatid cysts in children. 836 43

A 26-year-old man who had neurofibromatosis type-2 with symptoms of unexplained optic disc edema is reported. Magnetic resonance imaging (MRI) revealed bilateral acoustic schwannomas. Obstructive hydrocephalus, however, was not evident in spite of his severe disc edema and visual loss. After partial removal of the right acoustic schwannoma, symptoms of intracranial hypertension, such as vomiting and headache, developed and MRI demonstrated evidence of obstructive hydrocephalus. Placement of a ventricular-peritoneal shunt relieved the symptoms of intracranial hypertension, but visual acuity in his left eye was reduced to hand motion due to secondary optic atrophy. In patients with similar symptoms it is suggested that, in addition to tumor removal, early treatment to decrease intracranial pressure should be considered when visual function is progressively impaired by the symptoms of prolonged papilledema.
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PMID:Severe optic disc edema without hydrocephalus in neurofibromatosis 2. 982 67

We report a case of optic glioma with bilateral optic atrophy. A 3-year-old girl presented with vomiting and left hemiparesis. She had hypothalamic dysfunction, right ptosis, right monocular nystagmus, left facial palsy, left hemiparesis, and left pes adductus. Neuroimaging studies showed obstructive hydrocephalus with a large suprasellar calcified tumor with a ring-like enhancement mimicking craniopharyngioma. Visual-evoked potentials showed delayed latency of N75 in the right occipital lead. The tumor, a pilocytic astrocytoma in the right optic tract and chiasma, was partially removed via a right frontotemporal craniotomy. The right optic nerve had shrunk to half the normal diameter and became twisted downwardly. Intracranial pressure (ICP) increased to 40 cm H2O. The fundus had bilateral optic atrophy without disc swelling. To our knowledge, this is the first report of a lamina/dot sign of the optic disc in a small child with a brain tumor and a normal neuroretinal fiber layer. These ocular findings may result from possible interruption of the axonal flow caused by the tumor and not increased ICP.
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PMID:Optic glioma with characteristic bilateral optic atrophy in a 3-year-old girl. 1070 32

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63


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