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Query: UMLS:C0027497 (
nausea
)
23,468
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache,
nausea
, vomiting, diplopia,
ataxia
or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.
...
PMID:Papilledema: clinical clues and differential diagnosis. 154 98
A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone.
Nausea
, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait
ataxia
and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
...
PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49
A case of craniopharyngioma originating in the very unusual location of the posterior fossa is presented. The patient, a 23-year-old man, was operated on at another hospital when he was 3 years old for craniopharyngioma in the suprasellar area. There was no complaint for several years after this initial operation. Three months before he was admitted to our hospital, he had complaints of headache, vomiting,
nausea
, and
ataxia
. A computed tomographic scan revealed a mass with a cyst and calcifications in the posterior fossa. The tumor was removed totally.
...
PMID:Craniopharyngioma of the posterior fossa. 162 Mar 17
A 68-year-old woman had an abrupt onset of severe headache,
nausea
, vertigo, difficulty in standing and dysarthria. A CT scan of the brain disclosed bilateral symmetrical round infarctions involving the middle cerebellar peduncles. She exhibited marked limb
ataxia
, gait
ataxia
, dysarthria and transient gaze nystagmus. Occlusion of the right vertebral artery associated with a stenosis of the basilar artery just proximal to the origin of the anterior inferior cerebellar arteries shown in angiograms were thought to be the cause.
...
PMID:A case of bilateral cerebellar peduncle infarction. 194 54
We analysed two of our own and 21 patients described in the literature with listeria brainstem encephalitis. The disease was characterised by a prodromal state with fever,
nausea
and headache followed by severe brainstem dysfunction with multiple cranial nerve palsies,
ataxia
, respiratory insufficiency and coma. The diagnosis was established by isolation of Listeria monocytogenes from CSF and/or serum. Serological tests are without diagnostic evidence. Cerebrospinal fluid examination may not initially point to a bacterial infection. Computed tomography and magnetic resonance imaging technique might supply evidence of brainstem involvement and contribute to an early diagnosis. There is a high percentage of lethal outcome without early antibiotic therapy.
...
PMID:Listeria brainstem encephalitis: two own cases and literature review. 201 6
Pseudotumour was diagnosed in six patients aged 3-38 years during an 8 years period. The diagnosis was based on headache, papilloedema, normal CT scan and cerebrospinal fluid (CSF) composition. Additional clinical symptoms were
nausea
, VIth nerve palsy,
ataxia
, blurred vision and frank visual reduction over time. Sagittal sinus thrombosis was ruled out by angiography or magnetic resonance imaging. In five of the six patients lumbar steady state infusion tests were performed to evaluate intracranial hydrodynamics and CSF resorbtion. All patients demonstrated a markedly increased opening pressure (range 13 to 48 mm Hg). CSF outflow resistance ranged from upper normal to pathologically increased levels (8-19 mm Hg/ml/min). Combined epidural intracranial pressure/middle cerebral artery blood velocity monitoring in 3 patients revealed a great number of B waves and a labile cerebral vasomotor state. Pharmacological treatment was tried with digitoxin, acetazolamide, furosemide and/or corticosteroids. Two patients did well on long-term treatment with digitoxin and furosemide, respectively. In the other four patients the clinical development was unsatisfactory on medical treatment alone. They were subsequently operated with implantation of a lumboperitoneal, cisternoatrial or cisternoperitoneal shunt. Shunting rapidly reversed clinical signs and symptoms, except for a partial persistent visual loss in an 18 years old boy who had experienced symptoms for 3 years resistant to pharmacological treatment.
...
PMID:Pseudotumour cerebri-neurosurgical considerations. 208 40
Acute mountain sickness is a pathologic reaction as a result of bad adaptation to high altitudes (greater than 2.500 meters). The main symptoms are headache,
nausea
, vomits, and insomnia. When severe it can produce oliguria, retinal hemorrhage,
ataxia
and sometimes coma. Its etiology is not well known. It is considered that the first producer factor of the disease is tissular hypoxia secondary to low partial oxygen pressure existing in areas of high sea level. The treatment consists of descent and the use of dexametasone and acetazolamide.
...
PMID:[Acute mountain sickness]. 210 53
A 46-year-old healthy man suffered from sore throat, fever and right otalgia. On the next day, he developed hoarseness and difficulty in swallowing. On the 6th day, he suffered from vertigo, nausea and vomiting associated with unsteady gait. He was admitted to the otorhinolaryngology department in our hospital and pointed out to have vesicles at his right ear. On the 13th day, he was referred to our service. On admission, no vesicles were noted at the right ear or pharynx. Neurological examination revealed mild nuchal rigidity and marked hoarseness, associated with poor elevation of soft palate and loss of pharyngeal reflex on the right side. He also had horizontal-clockwise rotatory nystagmus in primary gaze and ataxic gait. There was no hearing loss nor facial palsy. No other abnormal neurological findings were noted. The cerebrospinal fluid showed pleocytosis associated with increased protein. The viral antibody titre for herpes zoster was significantly elevated on 18th day in serum as well as in cerebrospinal fluid. Vertigo,
nausea
, vomiting,
ataxia
and difficulty in swallowing were all disappeared by the 25th day, whereas hoarseness was improved but still noted 6 months later. Among cranial nerves, trigeminal and facial nerves are the most commonly affected in patients with herpes zoster, but there have been a few reported cases of the 9th and 10th cranial nerve involvement in the literature. In these previously reported cases, all were written before the era of serological diagnosis, and herpes zoster was diagnosed by the vesicles at the ear or pharynx.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[A case of unilateral VIIIth, IXth and Xth cranial nerve involvement with herpes zoster]. 216 88
Two hundred forty-one elderly depressed patients entered the 8-week, double-blind phase of this parallel-group, multicenter study; 161 patients were randomized to receive sertraline (50-200 mg/day) and 80 were randomized to receive amitriptyline (50-150 mg/day). Among evaluable patients, there were no statistically significant differences between treatments in any of the primary efficacy variables: change in total Hamilton Rating Scale for Depression (HAM-D) score (17 items), percentage change in HAM-D score, change in HAM-D Item 1, change in Clinical Global Impressions (CGI) Severity score, change in the Depression Factor of the 56-item Hopkins Symptom Checklist, and the CGI Improvement score at the last visit. Similar results were obtained using data from all patients (intention-to-treat analysis), except that amitriptyline was superior in HAM-D Total score (p = .044). The two drugs produced a similar degree of response: on the basis of the HAM-D criterion, 69.4% of sertraline patients and 62.5% of amitriptyline patients responded, and, on the basis of CGI criterion, 79.5% of sertraline and 73.4% of amitriptyline patients responded. Twenty-eight percent of the sertraline patients withdrew from the study because of a treatment-related side effect and 2.5% (4) because of a laboratory abnormality. In comparison, 35% of the amitriptyline patients withdrew because of treatment-related side effects. Sertraline was associated with a statistically lower frequency of somnolence, dry mouth, constipation,
ataxia
, and pain and a higher frequency of
nausea
, anorexia, diarrhea/loose stools, and insomnia; thus, anticholinergic effects were less common and gastrointestinal effects were more common with sertraline than with amitriptyline.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Double-blind, multicenter comparison of sertraline and amitriptyline in elderly depressed patients. 225 79
Dilantin toxicity has been well described and has generally been noted to include signs and symptoms of nystagmus,
ataxia
,
nausea
, and vomiting. Dilantin's depressive effects are seldom mentioned. Two patients are presented who, although stable while on the rehabilitation unit, developed vegetative signs of depression soon after discharge. Both were found to have toxic levels of Dilantin. Neither revealed the classic neurologic or gastrointestinal complaints. Although one patient had documented family and social stressors, the other had a stable home life. Both patients recovered remarkably once their Dilantin dosages were adjusted. In such patients who present with change in mood, sleeping, and eating patterns, Dilantin toxicity should be suspected. Serum blood levels should be checked, and dosage adjusted before the addition of antidepressant medication. Possible causes for Dilantin-associated depression are discussed in detail.
...
PMID:Dilantin toxicity and vegetative depression: a report of two cases. 224 39
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