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)

Two cases of traumatic aneurysm of peripheral cerebral artery were reported. Case 1. A 6-year-old girl was severely injured on her head by automobile accident. Plain skull films showed depressed fracture in the left frontal region. Left common carotid angiogram 25 days after the injury revealed small aneurysm of a cortical branch of the anterior cerebral artery. Cranioplasty and removal of the aneurysm was performed. Postoperative course of this patient was uneventful. Case 2. A 4-year-old girl fell downstaris and struck her left temporal region. On admission, she was unconscious and plain skull films showed multiple linear fractures. No aneurysm was demonstrated in the right common carotid angiogram immediately after the head trauma. Since her general condition gradually improved, she discharged 23 days after the head trauma. 63 days after the injury, she developed sudden onset of severe headache, vomiting, and status epilepticus. Right common carotid angiogram showed a large aneurysm arising from a branch of right pericallosal artery at the free edge of the falx. Parent artery of the aneurysm was clipped. Postoperatively, the patient made uneventful recovery. 60 reported cases of traumatic aneurysm of peripheral cerebral artery were reviewed and analyzed in etiology, diagnosis, clinical course, treatment and pathogenesis.
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PMID:[Traumatic aneurysm of the peripheral cerebral artery]. 103 73

A five-year-old male was admitted to the hospital with generalized seizures. Enlarged lymph nodes raised the suspicion of cat-scratch disease. The diagnosis was confirmed by a positive history of a cat bite, typical histopathologic findings in the biopsy of the lymph nodes, and a positive skin test. Brain CT scan and LP were repeatedly normal. The clinical course was remarkable for recurrent episodes of status epilepticus refractory to usual anticonvulsant therapy and prolonged encephalopathy consisting of mental confusion, hemiparesis, tremor, chorea, and vomiting. All neurologic symptoms gradually resolved within nine months, without sequelae. Cat-scratch encephalopathy should be suspected in a child presenting with status epilepticus and enlarged lymph nodes. Aggressive and prolonged anticonvulsant therapy is strongly recommended.
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PMID:Cat-scratch encephalopathy presenting as status epilepticus and lymphadenitis. 232 Apr 87

Continuous oculoclonic status epilepticus occurred for 90 min in a 4-year-old girl. The seizure consisted of continuous contralateral horizontal nystagmus concurrent with left occipital spike discharges, occasional vomiting and no loss of consciousness. Oculoclonic status epilepticus may be a variant form of versive status epilepticus.
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PMID:Oculoclonic status epilepticus. 291 13

Children with seizure disorders frequently are treated with anticonvulsant medications such as clonazepam, valproic acid, carbamazepine, and ethosuximide, which cannot be given parenterally. When the child is unable to take these anticonvulsants orally, he or she may be given parenteral doses of phenobarbital or phenytoin. In many cases, these two medications have failed previously to control seizures, leading to the use of the more recently developed drugs. The use of rectal preparations of some anticonvulsant medications is highly useful and effective when the child is unable to take oral medications because of repeated vomiting, gastrointestinal surgery, and status epilepticus associated with lack of venous access. Rectal use of anticonvulsants has a role in the management of hospitalized seizure patients and can be learned by parents needing to treat their children's seizures at home while awaiting other medical care.
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PMID:Rectal anticonvulsants in pediatric practice. 313 1

A 67-year-old man was admitted for status epilepticus, right hemiparesis, repeating vertigo and vomiting. Computed tomography showed no abnormality except for slight brain atrophy. Angiogram demonstrated bilateral vertebral artery stenosis at the origin, especially on the left side, and bilateral cervical internal carotid artery stenosis associated with ulceration. Intracranially, bilateral anterior cerebral artery was filled only by right internal carotid artery. Internal carotid artery on both sides did not fill the posterior cerebral artery. From these findings, we thought that both bilateral internal carotid artery and left vertebral artery should be surgically reconstructed. On June 4, 1986, left vertebral transposition to the common carotid artery and left carotid endarterectomy using double-balloon shunt were performed. Waiting for recovery of the general condition, right carotid endarterectomy was carried out on June 27, 1986. Postoperative angiogram demonstrated disappearance of bilateral internal carotid artery stenosis, and good filling of left vertebral artery through left common carotid artery. Postoperative course was uneventful and right hemiparesis gradually improved. Vertigo and vomiting completely subsided. The method and indication of combined reconstruction for extracranial vertebral and carotid artery were discussed.
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PMID:[A case of combined reconstruction of extracranial vertebral and carotid artery stenosis]. 337 49

Forty-five patients under the age of 20 years with rhinogenic subdural empyema were treated at Groote Schuur Hospital and Red Cross War Memorial Children's Hospital between 1979 and 1991. Thirty-two were male and 13 female. The majority were between 13 and 19 years of age. Headache was the predominant symptom in 41 patients. Vomiting occurred in 15 and 21 presented with seizures, 2 in status epilepticus. Thirty had swinging pyrexias and 26 neck stiffness while only 14 had focal neurological signs. Swelling of the face or orbit was seen in 24. Twenty-two had depressed levels of consciousness and 7 had Glasgow Coma Scale (GCS) values below 11/15. White cell counts and erythrocyte sedimentation rates were raised in all cases. Twenty-three patients underwent lumbar punctures despite the inherent danger in this procedure. Cerebrospinal fluid analysis showed a pleocytosis in all cases; no organisms were cultured in any of the specimens. The diagnosis in all cases was made by contrast-enhanced computed tomography. Twenty-five patients underwent multiple burrholes, 9 small craniectomies and 11 craniotomies. Thirty-four patients made an excellent recovery. All of the 6 patients who died had GCS values below 11 at the time of their surgery.
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PMID:Rhinogenic subdural empyema in older children and teenagers. 757 Feb 36

A 16-year-old female presented with clinical, morphologic and molecular features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Her early development was normal. Starting from the age of 14 years, she experienced recurrent episodes of headaches, with vomiting, seizures, transient right hemiparesis and decreased visual acuity. Computed tomographic brain scans revealed calcification in the bilateral basal ganglia. Biopsied specimens from her left biceps brachii and rectus femoris muscles revealed ragged-red fibers and strong succinate dehydrogenase-reactive blood vessels. Electron microscopy revealed paracrystalline inclusions in muscle mitochondria. Analysis of mitochondrial DNA (mtDNA) from blood, hair follicles and muscle specimens showed an A to G point mutation at nucleotide position 3,243 in the transfer RNA(Leu(UUR)). The proportion of mutant mtDNA in the patient's blood was 43%, in hair follicles 62% and in muscle 82%. The patient was followed up for 4 years and had progressive mental deterioration and died of an episode of status epilepticus. This patient and 5 other MELAS patients reported in Taiwan are compared.
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PMID:Heteroplasmic mitochondrial DNA mutation in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. 761 32

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46

A case is reported of a duodenal perforation by a Kimray-Greenfield filter hook in a 66-year-old female patient. This device had been inserted four years before, after a pulmonary embolism. The patient presented with epigastric pain, vomiting and extracellular dehydration with renal failure. A plain abdominal film showed the filter to be tilted 15 degrees to the left, with an opening 28 mm wide. Various investigations were carried out, none of which providing a satisfactory diagnosis. Steroid treatment (1 mg.kg-1 x day-1 of prednisone) was started before admission to intensive care. Only at that time gastroduodenoscopy showed on of the filter's hooks jutting through the duodenal wall. This perforation was located in the posterior wall of the third part of the duodenum, and was associated with an ulcer of the mucosa facing this hook. The diagnosis was confirmed by an abdominal CT scan. The hook was cut and the perforation sealed off during a first laparotomy. Twenty-six days later, the patient developed intestinal obstruction due to a haematoma of the jejunal wall. She later had a cerebrovascular accident, with status epilepticus and deep coma. She died four months after her admission. The late complications of vena caval filters are discussed. The position of these devices should be regularly checked by a plain abdominal film. Abdominal CT scanning is a useful investigation for the diagnosis of intra and extravascular complications.
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PMID:[Duodenal perforations by the hooks of a Kimray-Greenfield filter]. 833 71

A 78-year-old woman was admitted to our hospital because of disorientation and fever on January 21, 1992. Two days before admission she experienced vomiting, anorexia and general malaise. Laboratory examinations on admission disclosed a hemoglobin level of 11.1 g/dl and a platelet count of 8,000/microliters. The peripheral blood smear revealed anisocytosis with numerous schistocytes and poikilocytes. Polychromatophilic and nucleated red blood cells were also seen, and the reticulocyte count was 38/1000. Her serum lactate dehydrogenase (LDH) value was 2,977 WU and the total serum bilirubin level was 3.5 mg/dl with 2.7 mg/dl indirect reacting fraction. Serum creatinine was 4.7 mg/dl. Her consciousness became semicomatose after a systemic seizure which lasted approximately 15 seconds and her hemoglobin level decreased to 8.5 g/dl on hospital day 2. Therefore, we diagnosed her as having thrombotic thrombocytopenic purpura (TTP) because of the presence of all 5 features, that is, thrombocytopenia, microangiopathic hemolytic anemia, fluctuating neurologic abnormalities, renal dysfunction and fever. A plasmapheresis with fresh frozen plasma (FFP) replacement was begun on that day. She was also treated with anti-platelet agents, 80 mg/day aspirin, and 300 mg/day dipyridamole. Moreover, packed red blood cells (PRC) were infused. While also receiving diphenylhydantoin and phenobarbital to prevent convulsions, status epilepticus developed on day 3. Because of inhibited spontaneous respiration which was an adverse effect derived from diazepam and sodium thiamylal administered intravenously to treat the status epilepticus, an artificial respiration was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An elderly case of thrombotic thrombocytopenic purpura]. 848 87


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