Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective review was performed of the age profile and clinical features at presentation of 79 children with posterior fossa tumours. The mean age at presentation in this series (6.6 years) is consistent with a decreasing trend over the past 70 years. Headaches, ataxia and torticollis emerge as significant symptoms worthy of further investigation whilst abdominal pain and constipation might herald the presence of a posterior fossa tumour on rare occasions.
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PMID:Posterior fossa tumours in childhood: evaluation of presenting clinical features. 1132 Nov 74

Multiple complications of varicella have been described. Musculoskeletal complications (osteomyelitis, septic arthritis, and necrotizing fasciitis) as well as neurologic complications (ataxia, encephalitis, and transverse myelitis) are well-known. We describe the cases of 2 children, ages 18 months and 5 years, who were admitted recently to 2 pediatric hospitals in Montreal with a resolving varicella, abdominal and lumbar pain, and a refusal to walk and in whom a diagnosis of epidural abscess caused by group A streptococcus (GAS) was established. No previous case of epidural abscess caused by GAS in the context of varicella has been reported. Epidural abscesses are rare in pediatrics and are caused mainly by hematogenous spread of Staphylococcus aureus. The diagnosis in pediatrics is challenging because it is rare and does not present as classically as in adults. The prognosis is related to the presence of neurologic deficits before surgery and to the rapidity with which the diagnosis and the intervention are made. These cases highlight a new clinical association in children of epidural abscess caused by GAS and varicella. An early clinical diagnosis requires a high index of suspicion when back or abdominal pain with or without neurologic signs and symptoms occurs during or soon after varicella.
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PMID:Group a streptococcus spinal epidural abscess during varicella. 1177 82

Recurrent episodes of abdominal pain are common in childhood. Among the diagnostic possibilities are migraine and abdominal epilepsy (AE). AE is an infrequent syndrome with paroxystic episodes of abdominal pain, awareness disturbance, EEG abnormalities and positive results with the introduction of antiepileptic drugs. We present one 6 year-old girl who had short episodes of abdominal pain since the age of 4. The pain was followed by cry, fear and occasionally secondary generalization. MRI showed tumor in the left temporal region. As a differential diagnosis, we report a 10 year-old boy who had long episodes of abdominal pain accompanied by blurring of vision, vertigo, gait ataxia, dysarthria, acroparesthesias and vomiting. He received the diagnosis of basilar migraine. In our opinion, AE is part of a large group (partial epilepsies) and does not require a special classification. Pediatric neurologists must be aware of these two entities that may cause abdominal pain.
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PMID:Recurrent abdominal pain: when should an epileptic seizure be suspected? 1224 4

Here, we describe a 20-yr-old woman with COACH syndome (hypoplasia of Cerebellar vermis, Oligophrenia, congenital Ataxia, Coloboma, and Hepatic fibrosis) developing multiple liver lesions. Epigastric and right upper abdominal pain and lack of appetite led to clinical evaluation. Liver function tests showed an increase in transaminases and cholestatic parameters; alpha-fetoprotein was in the normal range. Ultrasound and magnetic resonance imaging examinations revealed multiple liver lesions. Histological examinations of ultrasonographically guided biopsies were consistent with regenerative hepatic nodules without features of malignant or dysplastic cells. The sizes of these tumors did not change over a period of 12 months. Our report presents the 10th case of COACH syndrome with a hitherto undescribed association with hepatic tumors.
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PMID:COACH syndrome associated with multifocal liver tumors. 1238 58

Whipple disease is an uncommon chronic bacterial infection due to Tropheryma whipplei. Clinical manifestations are protean (joint pain, fever, weight loss, abdominal pain, lymphadenopathies), and the diagnosis is often delayed. Although previously considered a late manifestation of Whipple disease, neurological involvement is now frequently the initial clinical manifestation and represents the greatest risk for long-term disability. All patients should be treated and monitored as if they had central nervous system disease even if they are asymptomatic. Neurological manifestations include dementia (56 percent), abnormalities of eye movements (33p. cent), involuntary movements (28 percent), seizures, hypothalamic dysfunction, myelopathy, ataxia and psychiatric manifestations. Uveitis, retinitis, optic neuritis and papilloedema may be found. 80 percent of the reported cases of neuro-Whipple had associated systemic symptoms or signs but many patients are presenting without concurrent intestinal manifestation. Thus, the disease may remain undiagnosed or misdiagnosed, as rheumatoid arthritis or sarcoidosis. Traditionally, the diagnostic procedure of choice is biopsy of the duodenal mucosa by demonstrating PAS-positive foamy macrophages. However, not all cases have small bowel infiltration and tissue obtained from sites clinically affected may be helpful. CT and MR images of the central nervous system are normal or not specific: atrophic changes, mass lesions, focal abnormalities and hydrocephalus. The application of a PCR assay against Tropheryma whipplei has transformed the diagnosis. Positive results have been obtained from several tissues and from CSF and PCR is more sensitive than other techniques. All patients must be treated with antibiotics which cross the blood-brain barrier. Most agree that initial treatment with a combination of parenteral penicillin and streptomycin for at least 14 days is appropriate, thereafter cotrimoxazole orally 3 times a day for at least one and probably for two years. Third generation cephalosporins, rifampicin and chloramphenicol have been used successfully. PCR is recognized to be a useful tool for monitoring progress but it is sometimes difficult to reverse established neurological defects.
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PMID:[Neurological manifestations of Whipple disease]. 1240 8

Salt poisoning has been described under various circumstances in adult cattle. Presenting clinical signs in 6 Holstein beef cattle with such poisoning were primarily dysfunction of the central nervous system and included ataxia, opisthotonus, nystagmus, depression, muscle twitching and intermittent convulsions, as well as abdominal pain and polydipsia. Diarrhea occurred in 2, and blindness in 3/6 cattle. Hypernatremia (161.8 - 178.8 mmol/L) and hyperosmolality (331.81 - 366.18 mOsm/L) were present in all animals. To treat the affected cattle, access to fresh water was restricted, vascular volume was expanded with isotonic saline and then hypotonic fluid (5% Dextrose solution) i.v. and dexamethasone im was administered. Although biochemical parameters returned to normal reference ranges, 3/6 affected animals remained blind.
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PMID:Salt poisoning in beef cattle. 1508 Feb 19

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
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PMID:Poisoning due to chlorophenoxy herbicides. 1557 61

A 6-year-old Quarter Horse stallion was referred to Oklahoma State University Veterinary Medical Teaching Hospital for evaluation of abdominal pain that developed after breeding activity earlier in the day. The horse developed diarrhea and progressively worsening neurologic signs (circling, ataxia, head pressing) within 22 hours of presentation and was subsequently euthanized due to severe self-destructive behavior. Antemortem biochemical and hematologic abnormalities included hypocalcemia but no evidence of hepatic disease. Idiopathic hyperammonemia and encephalopathy were suspected; cerebrospinal fluid (CSF) and aqueous humor were collected 10 hours postmortem for ammonia analysis using a colorimetric assay. Results were compared with those of 6 horses that also had been euthanized, for diseases unrelated to encephalopathy. Ammonia also was measured in plasma samples obtained antemortem. Ammonia concentrations in plasma (958 micromol/L), CSF (1566 micromol/L) and aqueous humor (1018 micromol/L) samples from the stallion were markedly increased compared to those in the 6 unaffected horses (plasma, 9-43 micromol/L; CSF, 370-532 micromol/L; aqueous humor, 70-483 micromol/L). Since the acute nature of hyperammonemic encephalopathy often does not provide sufficient time for an antemortem diagnosis, postmortem analysis of CSF and aqueous humor ammonia concentrations may be a useful alternative for documenting hyperammonemia in horses.
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PMID:Postmortem diagnosis of idiopathic hyperammonemia in a horse. 1752 96

We present a case of a 4-year-old who presented to the emergency department with an unsteady gait for 2 days. Ataxia is a rare but known manifestation of cerebellar involvement in Lyme disease. A 4-year-old (17 kg) boy with no significant medical history presented to the emergency department (ED) with history of nonbloody emesis for 2 weeks and an unsteady gait for 2 days. Over the past 2 days, his gait had gotten progressively worse until he was unable to walk without assistance. The vomiting would usually occur 1 hour after eating meals. He had also complained of a single headache, which occurred approximately 10 days before admission. The headache did not occur in the early morning hours or wake him up from his sleep. His appetite for the weeks before admission had progressively decreased, and he had also become more irritable, especially when stimulated. He had increased fatigue for the week before presentation. His parents denied any fever, rhinorrhea, cough, diarrhea, rash, bruising, bleeding, or hematuria. The patient denied any abdominal pain or headache while in the ED.
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PMID:Acute ataxia in a 4-year-old boy: a case of Lyme disease neuroborreliosis. 1909 Dec 90

Ciguatera toxicity is a poisoning from consuming reef fish that had fed on dinoflagellates such as Gambierdiscus toxicus found along coral reefs. The toxin is oil soluble, odorless, colorless, tasteless, heat stable, and is concentrated in larger carnivorous fish such as amberjack, barracuda, eel, grouper, red snapper, sea bass, and Spanish mackerel. Onset of symptoms is usually within 6-12 hours after ingestion. Gastrointestinal symptoms lasting 1-2 days include abdominal pain, nausea, vomiting, and diarrhea. Neurological symptoms may persist for weeks or several months or--rarely--years and include circumoral and extremity paresthesias, temperature sensation reversal, itching, weakness, ataxia, and others. A patient with burning hands and feet who had not found relief using other methods had diagnosis of ciguatera toxicity assisted by hypnotically refreshed memory followed by rapid relief with hypnotic suggestions in 1 session and remained free of symptoms.
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PMID:Hypnosis to alleviate the symptoms of ciguatera toxicity: a case study. 2244 20


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