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)

A 13 1/2-month-old boy with severe microcephaly was found to have nearly total absence of the telencephalon. The patient had marmorated skin, hypoplastic penis and undescended testes. Spastic tetraparesis was present. Moro, grasp and sucking reflexes were easily elicited. He could not sit or stand, but was able to raise and support his head. He had occasional convulsions and a tendency to hypothermia and vomiting. The EEG showed symmetrical low-voltage theta-delta activity. His psychomotor development was severely retarded. Bone age was normal. Head circumference was 28cm at six months and did not increase after this age. At autopsy the small cranial vault and meninges were found to be intact. Brain weight was 105g. The supratentorial part of the brain was extremely small, consisting of an irregularly lobulated mass about 3cm in diameter and without any median fissure or ventricular cavity. The telencephalon was severely involved and partly replaced by gliomesenchymal scar tissue, while the diencephalic structures, including the eyes and the optic nerves and chiasm, were comparatively well-developed. The cerebellum and brain stem were essentially intact.
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PMID:Atelencephaly. 91 6

Bilateral putaminal necrosis is characteristic of methanol poisoning. A 31-year-old male alcoholic had headache, impaired consciousness, neck stiffness, roving eyes with dilated unreactive pupils, papilloedema, abdominal pain, vomiting, and severe metabolic acidosis after a binge. Abnormalities of the cerebrospinal fluid included an initial pressure of 240 mmH2 O, RBC 286/mm3, WBC 8/mm3, and protein 179 mg/dl. Peritoneal dialysis was performed on the 2nd day after drinking. A blood test for methanol was not performed until the 5th day, and its results was negative. However, computed tomography (CT) on the 3rd day showed necrosis and hemorrhage of bilateral putamina and the cerebral cortex, and post-contrast enhancement of meninges. On the 22nd day, a CT revealed further changes: necrosis of bilateral subcortical white matter, and post-contrast gyral enhancement at the otherwise normal-looking areas of the cerebral cortex. We suggest that, in certain situations, the characteristic CT findings are helpful in the diagnosis of methanol poisoning.
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PMID:Bilateral putaminal necrosis caused by methanol poisoning: a case report. 131 54

Recognition of adrenal atrophy during a review of autopsy findings in two sisters who died at 8 months and 3 1/2 years prompted estimation of very long chain fatty acids, phytanic acid and pristanic acid on wet liver fixed in formalin for 12 years. These were shown to be markedly increased and defects in multiple peroxisomal functions and decrease in particulate catalase were shown in cultured fibroblasts, confirming an abnormality of peroxisomal biogenesis. The patients had presented with failure to thrive, recurrent diarrhoea and vomiting, poor mental development, retinal pigmentation, blindness and in the older patient deafness, with only mild dysmorphic features. Autopsy in the older patient showed adrenal atrophy, cirrhosis, and foamy histiocytes in multiple organs. The brain showed no demyelination, little cytoarchitectural abnormality, occasional perivascular histiocytes in the grey matter and meninges and prominent Purkinje cells in the molecular layer of the cerebellum. In the younger patient the changes were very subtle in spite of the marked clinical similarity. Despite the young age at death the clinicopathological features are most suggestive of infantile Refsum disease. In many situations anatomical pathology can be very useful in the recognition and study of peroxisomal disorders.
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PMID:Autopsy findings in two siblings with infantile Refsum disease. 137 19

A 13 year old boy died after a three day illness with severe headache, explosive vomiting, fever and progressive loss of consciousness. The autopsy revealed purulent and necrotizing meningoencephalitis mainly involving the basal regions and posterior fossa and on microscopic examination numerous trophozoites of Naegleria were seen in the meninges and necrotic brain tissue. The trophozoites were identified as Naegleria fowleri by immunoperoxidase staining. This case as well as others previously reported in Mexico and the documented presence of Naegleria species from several sources indicate that primary amebic meningoencephalitis should be considered in the differential diagnosis of cases with neurological symptoms of sudden onset.
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PMID:[Primary amebic meningoencephalitis caused by Naegleria fowleri in an adolescent from Huetamo, Michoacan, Mexico]. 260 77

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

A four - month old boy with Salmonella Typhimurium meningitis is presented. This patient was admitted to the hospital with a diagnosis of staphylococcal pneumonia, pyo-pneumothorax, cardiac failure and anemia. He has been treated for 18 days and he was discharged in good condition. Two days after discharge patient was readmitted with a fever, vomiting and feeding problem. In physical examination, stiff neck and bulging of the fontanel were remarkable. Examination of cerebrospinal fluid (CSF) has revealed meningitis and cultures of blood and CSF specimens were positive for S. typhimurium. It was sensitive only to trimethoprim sulphamethoxazole and netilmicin. Trimethoprim sulphamethoxazole (IM) and netilmicin (IV) were given. At the fifth day of this treatment patient expired. Postmortem examination has revealed the same agent in both meninges tissue and CSF cultures.
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PMID:[Salmonella meningitis]. 636 87

We report an autopsy case of granulomatous angiitis of the central nervous system (GANS) complicated by the syndrome of inappropriate antidiuretic hormone (SIADH). A 88-year old female was admitted because of progressive mental deterioration, fever, and vomiting. A computed tomogram disclosed bilateral periventricular lucency, and a low-density area in the right occipital lobe. Laboratory studies during her hospital stay, revealed hyponatremia, hypoalbuminemia, and increased antidiuretic hormone. Treatment with antibiotics, hypertonic saline solution, and steroids, and water restriction was ineffective, and the patient died six weeks after admission. Autopsy examination of the brain revealed slightly turbid meninges with multiple small infarctions in the corona raiata of both cerebral hemispheres. Microscopic study disclosed granulomatous inflammation with many giant cells in the walls of small and medium sized vessels, and the adventitia and media were more involved than the intima. Their lumens were narrowed, and many thrombi were observed. Extensive non-granulomatous inflammatory change was found mainly in the subarachnoid space. All of these findings were similar to the GANS firstly reported by Cravioto et al, in 1959. Since the blood vessels in the central nervous system play an important part in any inflammatory conditions and the blood vessels may be involved by bacterial, fungal, parasitic or viral meningitis, various microorganisms have been suspected as the cause of GANS, including mycoplasma, herpes zoster, herpes simplex viruses, cytomegalovirus, and human T-lymphotropic virus type III (HTLV-III). Some reported cases have been associated with Hodgkin's disease and cerebral amyloid angiopathy. We could not identify any cause in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Granulomatous angiitis of the central nervous system complicated by the syndrome of inappropriate antidiuretic hormone]. 760 90

From records on the clinical course of 699 military and veteran patients who had coccidioidomycosis before the advent of effective antifungal therapy, we identified 25 cases in which the manifestations of meningeal dissemination were described. Of 21 patients who had an identifiable initial infection, 16 developed meningeal symptoms (most frequently headache, vomiting, and nuchal rigidity) within the next 6 months. Associated pulmonary lesions were significantly more frequent in the right than in the left lung, as was also the case among 47 matched control patients who had coccidioidomycosis but not meningitis. Of 17 patients whose meningeal symptoms developed during the period studied, all died within 31 months. However, four of eight patients whose onset of symptoms preceded the study period survived for 55-146 months. Patients whose extrapulmonary dissemination involved only the meninges survived significantly longer than did those with more extensive infections. Even without therapy, the white blood cell count in cerebrospinal fluid markedly decreased during the course of the infection. The quantitative analysis provided herein offers a basis for meaningful comparisons with patients enrolled in current and future trials of therapy for coccidioidal meningitis.
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PMID:The natural history of coccidioidal meningitis: VA-Armed Forces cooperative studies, 1955-1958. 844 3

A nine months old boy was admitted to the hospital with the diagnosis of meningoencephalitis 15 days after having a clinically diagnosed chickenpox. Lumbar puncture showed clear CSF with 0.23 g/l of proteins, 57 mg/dl of glucose, 30 red cells/mm3 and 5 leukocytes/mm3. Blood count showed a packed red cell volume of 22%, a hemoglobin of 7 g/dl, 14800 leukocytes with 1% eosinophils, 5% band and 39% segmented neutrophils, 50% lymphocytes and 5% monocytes and a decreased platelet count. On the fourth hospitalization day, the patient had vomiting, irritability and stiff neck. A new lumbar puncture showed a clear CSF that differed from the former only in the glucose level that increased to 102 mg/dl. The patient died and the necropsy showed a congestive and enlarged brain and congestive meninges infiltrated with lymphocytes. There was lymphoid follicle hyperplasia in the small bowel and enlarged mesenteric lymph nodes. Samples of brain, brain stem, spinal cord and stools were sent for virological study. A Coxsackie B-5 virus was isolated from the spinal cord sample.
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PMID:[Isolation of Coxsackieviruses B5 in a fatal case of meningoencephalitis]. 873 69

We reported a case of spontaneous intracranial hypotension (SIH) who exhibited a remarkable leakage and collection of CSF in the spinal vertebral column. A 28-year old woman suddenly developed a severe occipital headache and vomiting. She had no headache while lying, but the headache was severe while sitting and standing. She had no recent history of trauma, but she fell down and hit her neck while skiing 6 months before the onset of headache. Neurological examination, urine and blood tests failed to reveal abnormal findings. Lumbar puncture showed a very low CSF pressure of 10 mmHg. Brain MRI demonstrated diffuse thickening and contrast enhancement of the meninges and spinal MRI displayed a CSF collection in the epidural spaces. RI cisternography showed a CSF leakage and an early accumulation of isotope in the kidneys and urinary bladder. Myelography revealed a CSF leakage at the C2 level from the spinal sac out to the extravertebral tissue and a CSF collection in the epidural spaces in the cervical to lumbar spinal canal. The root sleeves were also visualized by the CSF leakage. Thus, we demonstrated in this patient with SIH the location of CSF leakage at C2 dural sac and an extensive collection of leaked CSF in the epidural spaces, which apparently played a role in the occurrence of SIH.
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PMID:[A case of spontaneous intracranial hypotension with a remarkable leakage and collection of CSF]. 1061 60


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