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)

The characteristics of common migraine are not unique, they also appear in other forms of benign headaches. As there are no laboratory tests and biological signs enabling the diagnosis of migraine and its differentiation from the headache due to muscle contractrion, clinical criteria which are simplified and easy to comprehend should be used. We compared the symptoms in 29 patients of both sexes, suffering from common migraine, as well as 29 patients with headache due to muscle contraction (chronic daily headaches). In common migraine the following symptoms appear in greater percentage (statistically significant): nausea, vomiting, unilateral localization of pain, pulsating pain, photophobia and phonophobia. Bad headache is more frequent in patients with common migraine than in those suffering from chronic headache. We should accept Solomon's and Cappa's attitude who suggest at least two of the following five criteria: 1. nausea with or without vomiting, 2. unilaterality, 3. pulsating pain, 4. photophobia or phonophobia, and 5. provocation by menstruation or positive family history. Besides the above mentioned criteria the authors also mention and emphasize the existence of free interval in migraine when the patient has no difficulties and feels well.
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PMID:[Common migraine--diagnostic criteria]. 226 10

A 59 year-old female with hypercereatinekinasemia associated with pituitary apoplexy was presented. The patient showed headache, nausea, vomiting and pyrexia. On admission, slight nuchal rigidity and photophobia were observed. However all the cranial nerves were intact; neither ophthalmoplegia nor visual defect were observed. Cerebrospinal fluid analysis revealed an elevated protein concentration of 164 mg/dl. There were 157 cells/mm2 (30% neutrophils). Skull X-P disclosed the ballooning of the sella turcica. CT scan, endocrinological examination and angiography lead us to the diagnosis of pituitary apoplexy. By the sphenoidal approach necrotic tissue with a little chromophobe adenoma were removed. No haematoma was detected. The isozyme pattern of serum CK showed 100 percent MM type. Serum CK concentration reached as high as 2502 IU/l on the fifth day from the onset of the symptom and then normalized in 12 days. Though the cause of the hypercreatinekinasemia uncertain, the similar pattern of hypercreatinekinasemia is known in the acute stage of cerebrovascular accident, and it is more often observed in thalamic hemorrhage. We assumed that the hypercreatinekinasemia in our case was caused by hypothalamic irritation, which lead hyperpermeability of sarcolemma and leakage of the enzymes of muscle origin.
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PMID:[Pituitary apoplexy with hypercreatinekinasemia]. 235 Sep 34

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

A multicenter, randomized, double-blind trial was conducted to compare the efficacy of Cafergot P-B with that of its components, Cafergot, pentobarbital, and Bellafoline, and with placebo for the treatment of migraine. Patients with vascular headaches of the migraine type who regularly experienced nervous tension and some form of gastrointestinal distress with their headaches were randomized to one of five treatment groups. They were given treatment packets containing their assigned drug for use during two separate migraine attacks. Patients made pretreatment evaluations of the following symptoms: head pain, nervous tension, nausea, vomiting, anorexia, abdominal cramps, and photophobia. They made posttreatment evaluations of these symptoms 0.5, 1.0, 1.5, 2.0, and 3.0 hours after ingesting their assigned drug. Improvement scores were calculated from the differences between the pretreatment and the posttreatment ratings. Patients also made a final global assessment of their drug's efficacy. All patients who took at least one dose of the study medication and completed a baseline evaluation and at least one postdose evaluation of severity of pain were included in the analysis (n = 254). The comparisons of particular interest were those between Cafergot P-B and Cafergot and between Cafergot P-B and placebo. Cafergot P-B was significantly more effective than Cafergot in relieving head pain at hours 2 and 3, nervous tension, nausea, vomiting, anorexia, and photophobia. Cafergot P-B was significantly more effective than placebo in relieving head pain, nervous tension, nausea (second headache only), vomiting, and photphobia. The incidence of reported adverse effects was no greater with Cafergot P-B than with Cafergot; however, patients given Cafergot P-B reported less vomiting than did patients given Cafergot. The results of this study show that addition of pentobarbital and Bellafoline to Cafergot provides greater relief of pain, vomiting, nervous tension, photophobia, and other symptoms associated with migraine, while reducing the severity of the nausea that may accompany a migraine headache or Cafergot therapy.
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PMID:Symptomatic relief of migraine: multicenter comparison of Cafergot P-B, Cafergot, and placebo. 249 84

An epidemic of group A meningococcal disease began in Auckland in May 1985. There were 122 paediatric cases of meningococcal disease in the next 25 months including 98 cases due to group A. The commonest clinical symptoms were vomiting, headache and photophobia, while frequent signs included fever, seizures, petechial rash and meningism or a bulging fontanelle. Complications were uncommon and included sterile arthritis and prolonged fever. The majority had disease confirmed by positive blood or cerebrospinal fluid culture. Significantly fewer positive cultures were seen in those treated with antibiotics prior to admission. The overall mortality was 7%. If the acute illness was survived, the only detected long term sequela was sensorineural hearing loss seen in 6%. A vaccine programme has been undertaken to control this epidemic.
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PMID:The clinical features of paediatric meningococcal disease Auckland, 1985-87. 249 88

Subcutaneous GR43175 was examined in patients with acute migraine for efficacy, tolerability and safety in an open, controlled, dose-ranging study. Ten patients with acute, non-medicated, migraine (15 attacks) were assessed for severity of headache and associated symptoms (nausea, vomiting and photophobia). GR43175 plasma samples were monitored serially after dosing. Doses of 2 mg or 3 mg gave rapid relief of all migraine symptoms. Thirteen attacks (86%) had either resolved completely or improved to a mild non-migraine residual headache within 40 min. Treatment was well tolerated at all doses, the only adverse effects being transient pain on injection. Peak plasma concentrations were obtained within 10-20 min; a decline in plasma drug concentration did not result in a relapse in headache severity.
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PMID:Initial clinical experience with the use of subcutaneous GR43175 in treating acute migraine. 254 88

Headaches affecting 117 insulin-dependent diabetic patients were studied. 50 developed 3 varieties of headaches associated with clinical hypoglycaemic episodes: (1) Brief headaches, contemporaneous with cerebral and autonomic symptoms, were relieved within minutes of ingesting carbohydrates (8 patients). (2) Prolonged headaches outlasting hypoglycaemic symptoms by 1-48 (average 4.3) hours, not relieved by food, occurred in 36 patients; 12 of these also had nausea, vomiting or photophobia. (3) Migraine headache. 11 of the 117 patients were migraineurs: in 6 of the 11 their typical migraines (2 classical and 4 common) were induced by hypoglycaemic episodes. 9 of the 50 had 2 types of headaches, easily distinguished by each subject. In the whole series of 117 patients, 9 had never had a headache in their life. The remainder had headaches associated with premenstrual tension, anxiety, alcohol or other causes.
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PMID:Headaches in insulin-dependent diabetic patients. 261 15

One hundred epileptic patients were questioned about their headaches. Post-ictal headaches occurred in 51 of these patients and most commonly lasted 6-72 hours. Major seizures were more often associated with post-epileptic headaches than minor attacks. Nine patients in this series of 100 also had migraine: in eight of these nine a typical, albeit a mild, migraine attack was provoked by fits. The post-ictal headache in the 40 epileptics who did not have migraine was accompanied by vomiting in 11 cases, photophobia in 14 cases and vomiting with photophobia in 4 cases. Furthermore, post-epileptic headache was accentuated by coughing, bending and sudden head movements and relieved by sleep. It is, therefore, clear that seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics. It is proposed that post-epileptic headache arises intracranially and is related to the vasodilatation known to follow seizures. The relationship of post-epileptic headache to migraine is discussed in the light of current ideas on migraine pathogenesis, in particular the vasodilation which accompanies Leao's spreading cortical depression.
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PMID:Post-epileptic headache and migraine. 311 78

A case of traumatic low pressure headache syndrome after a fall on the buttocks is described. This rare syndrome is probably caused by unusual cerebrospinal fluid leakage. The headaches are characterized by accentuation in the erect position and relieved by recumbency, and may be associated with nausea, vomiting, dizziness, photophobia and vertigo. Carefully executed lumbar puncture in the lateral recumbent position shows absent CSF pressure and even spontaneous aspiration of air through the lumbar puncture needle. Intracranial air resulting from puncture may be demonstrated on routine roentgenogram. In computed tomography the syndrome is associated with extremely small ventricles and tight basal cisterns. Management consists in bedrest and fluid substitution.
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PMID:[Post-traumatic hypoliquorrhea syndrome]. 318 78

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17


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