Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brucellosis is a common zoonosis in many parts of the world, including Mediterranean and Middle Eastern countries. The disease is primarily related to occupations at risk, such as veterinarians, farmers, laboratory technicians, abattoir workers, and others working with animals and their products. Neurologic complications of brucellosis are quite rare, ranging from 1.7 to 10% of those infected. To date, no cases of neurobrucellosis with hydrocephalus have been reported. A 38-year-old right-handed farmer complained of headaches, nausea, vomiting, gait disturbance, and sweating for 2 days. He also complained of bilateral hearing loss of 4 months duration. On neurologic examination, dysmmetry, dysdiadochokinesis, ataxia on the left, and bilateral sensorineural hearing loss existed. On cranial MRI, a communicating hydrocephalus was noted. Because the patient consumed fresh sheep cheese and was a farmer, brucellosis was considered in the differential diagnosis. Brucella agglutination was positive with a 1/320 titer in the blood and a 1/80 titer in the cerebrospinal fluid. Ceftriaxone, doxycycline, and rifampicin were administered and by the fourth week of treatment, the ataxia was markedly improved, and the patient was able to walk without support. His cranial MRI demonstrated a total regression of the hydrocephalus. As a result, we suggest that neurobrucellosis should be considered in patients with hydrocephalus, especially if they live in an endemic area for brucellosis, even in the absence of other systemic signs.
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PMID:First case report of neurobrucellosis associated with hydrocephalus. 1849 39

Methyl bromide is a highly toxic gas with poor olfactory warning properties. It is widely used as insecticidal fumigant for dry foodstuffs and can be toxic to central and peripheral nervous systems. Most neurological manifestations of methyl bromide intoxication occur from inhalation. Acute toxicity characterized by headache, dizziness, abdominal pain, nausea, vomiting and visual disturbances. Tremor, convulsion, unconsciousness and permanent brain damage may occur in severe poisoning. Chronic exposure can cause neuropathy, pyramidal and cerebellar dysfunction, as well as neuropsychiatric disturbances. The first case of methyl bromide intoxication in Thailand has been described. The patient was a 24-year-old man who worked in a warehouse of imported vegetables fumigated with methyl bromide. He presented with unstable gait, vertigo and paresthesia of both feet, for two weeks. He had a history of chronic exposure to methyl bromide for three years. His fourteen co-workers also developed the same symptoms but less in severity. Neurological examination revealed ataxic gait, decreased pain and vibratory sense on both feet, impaired cerebellar signs and hyperactive reflex in all extremities. The serum concentration of methyl bromide was 8.18 mg/dl. Electrophysilogical study was normal. Magnetic resonance imaging of the brain (MRI) revealed bilateral symmetrical lesion of abnormal hypersignal intensity on T2 and fluid-attenuation inversion recovery (FLAIR) sequences at bilateral dentate nuclei of cerebellum and periventricular area of the fourth ventricle. This incident stresses the need for improvement of worker education and safety precautions during all stages of methyl bromide fumigation.
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PMID:Neurological manifestation of methyl bromide intoxication. 1857 99

The patient was a 70-year-old man with metastatic pancreatic cancer. After he received combination chemotherapy with gemcitabine and oral S-1 on day 1, he experienced severe general fatigue, anorexia and nausea. Then we changed the dose of gemcitabine from 1,000 mg/m(2) 2 to 500 mg/m(2) according to the criteria for an individual maximum repeatable dose (iMRD) determination method on day 8. His general condition recovered, and treatment schedule of gemcitabine with S-1 was continued sequentially at an outpatient clinic. His tumor marker levels, and the sizes of primary pancreatic tumor and liver metastatic lesions remarkably decreased. Partial response has been obtained for 7 months.
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PMID:[A case of advanced pancreatic cancer responding to combination chemotherapy with the individual maximum repeatable dose of gemcitabine and oral S-1]. 1863 36

Cyclic vomiting syndrome (CVS) is a disorder characterized by recurrent, stereotypic episodes of incapacitating nausea, vomiting, and other symptoms, separated by intervals of comparative wellness. Associated symptoms include nausea, abdominal pain, headache, and motion sickness. Recently, CVS was categorized as a migraine. Case 1 was a girl aged 4 years and 11 months, who had frequent and severe episodes of vomiting since she was 3 years old. The diagnosis of CVS was established on the basis of clinical symptoms and laboratory data. Her electroencephalogram was normal. Prophylactic therapy using a single drug such as amitriptyline, carbamazepine, phenytoin, cyproheptadine, valproate sodium or phenobarbital was not effective. However, her recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. Case 2 was a boy aged 10 years and 7 months, who had frequent episodes of vomiting since he was 1 year and 10 months old. He had been receiving intravenous hyperalimentation therapy at home since infancy because of frequent vomiting and failure to thrive. His electroencephalogram showed no abnormality. Prophylactic therapy using a single drug such as diazepam, phenytoin, valproate sodium or phenobarbital was not effective. However, his recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. There were no adverse effects in both patients. The combination therapy with valproate sodium (20 - 26 mg/kg/day) and phenobarbital (4 - 5 mg/kg/day) was effective as a prophylactic therapy in these two patients. The combination therapy with valproate sodium and phanobarbital for prophylaxis of vomiting may be helpful in patients with intractable CVS.
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PMID:[The effect of prophylactic therapy with valproate sodium and phenobarbital in two patients with cyclic vomiting syndrome]. 1880 88

We present an extremely rare autopsy case with traumatic dissection of the extracranial vertebral artery due to blunt injury caused by a traffic accident. The patient complained of nausea and numbness of the hands at the scene of the accident. His consciousness deteriorated and he fell into a coma within 12h, then died 4 days after the collision. Brain CT/MRI disclosed massive infratentorial cerebral infarction while MRA imaged neither of the vertebral arteries. Autopsy revealed a seatbelt mark on the right side of the lower neck, with fracture of the right transverse process of the sixth cervical vertebra. The right extracranial vertebral artery (V2) showed massive medial dissection from the portion adjacent to the fracture throughout the upper end of the extracranial part of the artery and was occluded by a thrombus. An intimal tear was confirmed near the starting point of the dissection. The brain disclosed massive infarction of posterior circulation territories with changes to the so-called respirator brain. The victim's left vertebral artery was considerably hypoplastic. We concluded that a massive infratentorial infarction was caused by dissection of the right extracranial vertebral artery and consecutive thrombus formation brought about by impact with the seatbelt at the time of the collision.
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PMID:Traumatic dissection of extracranial vertebral artery with massive subtentorial cerebral infarction: report of an autopsy case. 1926 36

Meckel's diverticulum (MD) is the most common congenital anomaly of the gastrointestinal tract, occurring in 2-3% of the population. Enterolith formation associated with MD is a rare entity. We present the case of a 35-year-old active duty sailor who presented with a 24-hour history of worsening abdominal pain and nausea. His exam revealed lower abdominal peritonitis. An abdominal and pelvic CT scan revealed a fluid-filled structure in the pelvis adjacent to the distal small bowel with associated calcifications. Exploratory laparotomy was performed, which revealed an acutely inflamed MD associated with enterolith formation. Consideration of this condition in the differential upon presentation of an acute abdomen is essential, secondary to the morbidity that can accompany it when misdiagnosed.
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PMID:Meckel's diverticulitis with associated enterloith formation: a rare presentation of an acute abdomen in an adult. 1935 4

Sevoflurane, a halogenated anesthetic, is associated with mild aminotransferase elevations but does not tend to cause clinically significant hepatotoxicity. We report a rare case of severe hepatic necrosis following exposure to sevoflurane during surgery. A 37-year-old man presented with nausea,vomiting, abdominal pain, and jaundice on the third postoperative day after an abdominal wall mass resection. Laboratory tests showed markedly elevated aminotransferase levels, hyperbilirubinemia, and coagulopathy. His viral hepatitis and human immunodeficiency virus (HIV) serologies were negative for acute infection, and his Epstein-Barr virus (EBV) and cytomegalovirus (CMV) serologies were suggestive of recent EBV infection and remote CMV infection. Antinuclear antibody and anti-smooth muscle antibody screens were negative. Ceruloplasmin and serum copper values were in the normal range. The histopathological findings included an acute centrilobular cholestatic hepatocellular injury compatible with the clinical history of acute drug-induced hepatotoxicity. The patient improved with conservative management. Unlike other halogenated anesthetics, proposed mechanisms of sevoflurane hepatotoxicity include production of compound A, increased cytosolic free Ca(2+), and activation of free radical metabolizing enzymes. The patient was likely susceptible to toxicity due to an underlying EBV infection and a probable history of exposure to halogenated anesthetics. Sevoflurane is generally considered to be relatively safe for subjects with mild liver dysfunction, in comparison with other halogenated anesthetics. However, this case suggests that sevoflurane can lead to severe life-threatening hepatic necrosis in at-risk individuals.
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PMID:Sevoflurane hepatotoxicity: a case report of sevoflurane hepatic necrosis and review of the literature. 1945 19

A 34-year-old man was admitted with his unsteady gait, difficulty in speech and a paroxysmal severe headache accompanied with sensori-motor disturbance of the right extremities and aphasic symptom. His family history was unremarkable. His unsteadiness has progressed very slowly from childhood. He noted to be inarticulate at the age of 18 years. At the age of 33 years, he suddenly had an attack of severe throbbing headache, which was mainly left parietal, with nausea and photophobia. During the headache, his right extremities were paralyzed and he became aphasic. He had lost a partial memory of the event All these symptoms had gone within 24 hours. Thereafter, the same headache occurred about once a month. Neurological examination revealed a mild truncal ataxia and ataxic dysarthria. Electroencephalography (EEG) showed intermittent delta waves restricted over the left fronto-temporal region. Brain MRI showed a moderate atrophy of superior cerebellar vermis and anterior cerebellar lobe. The diagnosis of sporadic hemiplegic migraine (SHM) with cerebellar ataxia was made. Our case was very similar to familial hemiplegic migraine (FHM) 1, of which some families are accompanied with transient amnesia, cerebellar ataxia and EEG abnormality. Although we did not detect any mutations in CACNA1A gene previously reported in FHM1, our case might share same pathogenesis with FHM1.
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PMID:[Case of sporadic hemiplegic migraine with cerebellar ataxia]. 1959 4

The principal toxic ingredients of aconite roots include aconitine, mesaconitine and hypaconitine, which are known cardiotoxins and neurotoxins. A 58-year-old man took a decoction of 11 g each of processed 'chuanwu' (the main root of Aconitum carmichaeli) and processed 'caowu' (the root of A. kusnezoffii) as treatment for his neck pain. One hour later, he experienced numbness of tongue and the four limbs, generalized weakness, nausea, vomiting, diarrhoea and dizziness. Three hours after ingestion, he was admitted to hospital. His blood pressure was 106/53 mmHg and heart rate 65 beats/min. Six hours after ingestion, he became hypotensive (systolic blood pressure <100 mmHg) with bradycardia (heart rate <60 beats/min). As treatments for the hypotension, he was given intravenous infusions of 0.9% saline (125 mL/hour) for 15 hours (7-21 hours after ingestion) and dopamine (3 microg/kg/min) for 36 hours (10-45 hours after ingestion). He was given atropine 0.6 mg intravenously 7 and 24 hours after ingestion. He was hypotensive for 31 hours (6-36 hours after ingestion), with a systolic blood pressure of 84-106 mmHg (mean 93.5) and a diastolic blood pressure of 40-59 mmHg (mean 51.8). He had bradycardia for 36 hours (6-41 hours after ingestion), with a heart rate of 45-68 beats/min (mean 56.5). On discharge (48 hours after ingestion), his blood pressure was 117/82 mmHg and heart rate 70 beats/min. In patients with aconite poisoning, prolonged hypotension and sinus bradycardia may occur and supportive therapy with close monitoring of blood pressure and cardiac rhythm are essential.
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PMID:Aconite poisoning presenting as hypotension and bradycardia. 1988 Jun 59

A 57-year-old heart transplant patient presented to the Emergency Department with mild epigastric pain, nausea, and vomiting for two days. Aside from a recent hospitalization for replacement of his hemodialysis catheter, he had otherwise not been ill. He was afebrile, slightly hypertensive, and slightly tachycardic with mild tenderness over the left upper quadrant, but no guarding, rebound tenderness, or masses. His WBC count was elevated at 16.1 (normal: 3.8-10.6). A computed tomography of the abdomen showed an area of low attenuation surrounding the aorta, surrounded more peripherally by an area of higher density. He went urgently to the operating room for a presumed contained rupture of the thoracic aorta. During the operation the surgeons noted inflammatory changes, rather than rupture, and resected and replaced the affected section. Cultures from a peri-aortic swab grew methicillin-resistant Staphylococcus aureus. Among complications of cardiac transplantation, aortic involvement can be a source of significant morbidity and mortality. Primary bacterial aortitis is, however, a rare event with instances of less than 3% in all patients. The presentation of these infections may be subtle, making diagnosis difficult and requiring a high index of suspicion. CT is the initial imaging technique of choice. Therapy frequently involves surgery in addition to broad-spectrum antibiotics. This patient's infection most likely originated from an infected dialysis catheter, the one that had just been replaced, and was probably kept from becoming more symptomatic by the administration of vancomycin during the previous admission.
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PMID:Methicillin-resistant Staphylococcus aureus aortitis in a cardiac transplant patient. 1993 90


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