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)

We report a 64-year-old man with recurrent bouts of blurred vision who died after developing an abdominal mass. He was well until June of 1985 when he was 59-years-old when he had an acute onset of loss of vision in his right eye. He was treated by prednisolone with a complete remission. In August of 1986, he had another bout of blurring of vision in his left eye. Once he lost his left vision completely, from which he showed slow recovery. In January of 1987, he developed blurring of his right eye and loss of pain and touch sensation in his right leg. Since then he repeated loss of vision in his right or left eye five times, and he was admitted to our hospital in May of 1990. On admission, he was alert and oriented. General physical examination was unremarkable. Neurologic examination revealed bilateral optic nerve atrophy. He could not discriminate light or dark by either eye. Other cranial nerves were unremarkable. He could walk in a wide-base only with support; spasticity was noted in his left leg. Muscle strength was preserved. Deep reflexes were exaggerated in both legs with extensor plantar reflex bilaterally. Pain and touch sensation was decreased in the left leg by 30%, and vibration was diminished in both feet. Position sense was preserved. Routine blood counts and chemistries were unremarkable. Cranial MRI scans revealed multiple high-signal intensity lesions in both pontine bases, basal ganglia, thalami, and in the deep cerebral white matters. He was treated with oral prednisolone, plasmapheresis, lymphocytapheresis, and then immuran. His vision showed only slight recovery to discriminate light and dark. In October of 1990, slight weakness appeared in his both legs. In December of that year, he developed nausea, and a fiber colonoscopic study revealed a stenosis in the transverse colon. In March of 1991, he developed anemia and liver dysfunction. In July of that year, jaundice appeared, and his serum bilirubin was increased. In October, his leg weakness became more prominent, and his cranial CT scans at that time revealed a low density change in the right cerebellum in the right superior cerebellar artery territory; in addition, multiple low density spots were scattered to be seen in both cerebral hemispheres including the basal ganglia and thalamic areas with ventricular dilatation and cortical atrophy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 64-year-old man with recurrent blurred vision and an abdominal mass]. 816 57

A 24-year-old oil well tester was rendered semiconscious by hydrogen sulfide (H2S). He received oxygen and was hospitalized but released in 30 minutes. The next day, nausea, vomiting, diarrhea, and incontinence of urine and stool led to rehospitalization. These problems and leg shaking, dizziness, sweating, trouble sleeping, and nightmares prevented his return to work. A physical examination, chest x-ray, and pulmonary function tests were normal 39 months after the episode but vibration sense was diminished. Two choice visual reaction times were delayed. Balance was highly abnormal (5 to 6 cm/sec) with eyes closed. Blink reflex latency was slow (R-1 17.5 msec versus normal 14.3 msec). Numbers written on finger tips were not recognized. Verbal and visual recall were impaired but overlearned memory was intact. Cognitive functions measured by Culture Fair, block design, and digit symbol were impaired. Perceptual motor was slow. Scores for confusion, tension-anxiety, depression, and fatigue were elevated and vigor was reduced. Forty-nine months after exposure his reaction time, sway speed, and color vision had not improved. His recall and his cognitive, constructional, and psychomotor speeds had improved but remained abnormal. These deficits are most likely due to H2S. Similar testing of other survivors is recommended.
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PMID:Case report: profound neurobehavioral deficits in an oil field worker overcome by hydrogen sulfide. 823 84

A case of aneurysms of bilateral distal posterior inferior cerebellar arteries (PICAs) is reported. A 61-year-old man experienced a sudden onset of headache and nausea and was admitted to a hospital immediately. His neurological examination showed no abnormalities, but headache and nausea continued in spite of conservative treatment. The patient was referred to our hospital two days after the onset and the neurological examination revealed slight dysmetria of the right upper extremity. A computed tomography (CT) scan demonstrated a round and heterogeneous high density mass at the cerebellar vermis and some blood coagula at the fourth ventricle and vermis. Angiography showed two aneurysms of the bilateral distal PICAs: The right aneurysm was at the cortical segment and the left one was at the telovelotonsillar segment. The patient underwent a suboccipital craniectomy and both aneurysms were clipped successfully. Sleepiness and headache continued postoperatively due to hydrocephalus. After ventricular drainage he soon recovered without having V-P shunt and was discharged with no neurological deficits. Aneurysms of bilateral distal PICAs are very rare and only three cases have been reported in the literature. The etiology, clinical symptom, CT finding and prognosis in the literature reviewed were briefly discussed.
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PMID:[A case of distal aneurysms of bilateral posterior inferior cerebellar arteries]. 832 59

Propionitrile, a substituted aliphatic nitrile commonly used in the chemical manufacturing industry, is capable of generating cyanide. However, there are few reports of human intoxication involving propionitrile. We report two workers at an organic chemical manufacturing plant who were overcome by fumes while treating a waste slurry into which unreacted propionitrile was discharged by mistake. One victim was comatose, acidotic, and hypotensive; his blood cyanide level was later measured at 5.0 micrograms/ml. He responded to sodium nitrite/sodium thiosulfate therapy by regaining consciousness. Continued symptoms were treated with hyperbaric oxygen at 2 atmospheres for a total of 4 hours. The second victim, who complained only of nausea, dizziness, and headache and who never lost consciousness, was treated with sodium nitrite/sodium thiosulfate. His measured blood cyanide concentration was 3.5 micrograms/ml. The ambient concentration of propionitrile in air samples at the work site shortly after the exposure was 77.5 mg/m3. In occupational situations in which workers exhibit rapidly progressive symptoms of headache, dizziness, collapse, and coma, and where substituted nitriles are known to be on site, acute cyanide poisoning should be strongly considered. Because of continued endogenous generation of cyanide from the metabolism of the parent compound, hyperbaric oxygen may be a valuable adjunctive therapy to consider, in addition to the immediate use of the cyanide antidote kit, in cases of poisoning by propionitrile or other substituted nitrile compounds. We urge the Occupational Safety and Health Administration to adopt workplace standards for the maximum ambient air concentrations for propionitrile.
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PMID:Successful treatment of life-threatening propionitrile exposure with sodium nitrite/sodium thiosulfate followed by hyperbaric oxygen. 788 67

A 46-year-old male presented with acute visual loss in the right eye, high fever, nausea, and vomiting. This was caused by herniation of the third ventricle into empty sella at 15 months of surgery for pituitary apoplexy. The sellar-suprasellar tumor was totally removed via a transcranial approach. Histological examination showed chromophobe adenoma with necrotic tissue, indicating pituitary apoplexy. His visual field defect worsened 15 months after the operation, and magnetic resonance imaging revealed moderate hydrocephalus and protrusion of the dilated anterior inferior portion of the third ventricle into the sella. The optic nerve, optic chiasm, and pituitary gland were compressed onto the sellar floor. Ventriculoperitoneal shunt relieved the visual impairment. A decompressive procedure such as ventriculoperitoneal shunts is a reasonable treatment for such a marked herniation of the third ventricle.
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PMID:Herniation of the third ventricle into empty sella caused by surgery for pituitary apoplexy--case report. 874 75

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68

A 25-year-old man developed nausea, vomiting, severe headache, and confusion. He had a past history of hyperuricemia and mild renal dysfunction. On admission he had somatic growth retardation, hypertrichosis, and bilateral auditory impairment. A cranial CT scan showed a small area of low density in the left temporal lobe and cerebellar atrophy. Five days later, he developed right homonymous hemianopia, sensory aphasia, and sensory inattention, and a new, large area of low density in the left occipital lobe on a cranial CT scan. On laboratory examination, lactate, pyruvate, and the lactate-to-pyruvate ratio were elevated in both the serum and cerebrospinal fluid. The biopsied muscle showed ragged red fibers and strongly SDH-reactive blood vessels. Gene analysis revealed the presence of the A 3243 G point mutation of the mitochondrial tRNA(Leu) gene in his blood leucocytes and muscle. Serum concentrations of BUN and creatinine were elevated to 46 mg/dl and 2.2 mg/dl, respectively. Creatinine clearance was 14.1 ml/min. An abdominal CT scan disclosed atrophy of his left kidney with subcapsular calcification and the findings of his abdominal ultrasonography were compatible with chronic renal failure. His mother, who suffered from renal failure and became dialysis dependent in her late forties also bore the A 3243 G mutation of the mitochondrial tRNA(Leu) gene in her circulating leucocytes. Though the association between MELAS and renal dysfunction still remains obscure, we speculate that renal failure can be a manifestation of MELAS.
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PMID:[Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with chronic renal failure: report of mother-child cases]. 897 30

A 15-year-old man was admitted because of diplopia and bilateral ptosis which occurred a few days after initial clinical signs, such as fever up, nausea, vomiting and headache. His pupils were anisocoric (Rt. phi 3.5 mm < Lt. phi 6.0 mm). In his left eye, light reflex was absent and its movements were limited in all directions. Brain MRI revealed the findings of paranasal sinusitis in bilateral ethmoidal and sphenoidal sinuses and swelling of bilateral cavernous sinus. Combination of intravenous antibiotic therapy and drainage improved his clinical symptoms and MRI findings. It was diagnosed as the inflammation originated in the sphenoid and ethmoid sinuses, which extended to the cavernous sinus and then involved III, IV, and VI cranial nerves. In conclusion, MRI was very useful to detect the cavernous sinusitis secondary to sphenoidal sinusitis.
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PMID:[A case of paranasal sinusitis-cavernous sinusitis with ophthalmoplegia externa]. 899 45

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
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PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

An 11-year-old boy suffered an inadvertent dural puncture during placement of an epidural catheter for postoperative analgesia. He developed symptoms of mild headache only, but severe and protracted orthostatic nausea and dizziness, which eventually resolved completely following epidural blood patch. His symptoms were atypical and could have been misinterpreted in the context of dural puncture for diagnosis, or for administration of intrathecal chemotherapy. The reported incidence of headache following dural puncture in children is low. It may be that the manifestations are different from those of adults and that the true incidence of symptoms related to leakage of cerebrospinal fluid is higher in children than currently recognised.
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PMID:Postdural puncture symptoms in a child. 924 30


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