Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 8-year-old girl living in rural southwestern Michigan experienced sudden onset of symptoms beginning with headache, dizziness and fever which rapidly progressed to central nervous system involvement with seizures and coma. Following 27 days of hospitalization her recovery was uneventful, with no apparent sequelae 15 months after discharge. Serologic studies of paired sera showed a rise in antibody to Jamestown Canyon virus, a member of the California serogroup (family Bunyaviridae). Specific IgM anti-Jamestown Canyon virus antibody was detected in sera drawn 9 days after onset. A concomitant rise in complement fixation antibody to herpesvirus was also noted. We believe this is the first reported case of encephalitis associated with Jamestown Canyon virus infection. Reasons are presented for the current inability to routinely detect infection and clinical illness caused by this virus.
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PMID:A case of encephalitis in a human associated with a serologic rise to Jamestown Canyon virus. 714 9

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

Syncope accounts for approximately 1% to 6% of hospital admissions and 3% of emergency room visits. Syncope is defined as a sudden transient loss of consciousness associated with a loss of postural tone with spontaneous recovery. Patients should not require electrical or chemical cardioversion to regain consciousness. Syncope must be clinically differentiated from other states of altered consciousness, such as dizziness, vertigo, seizures, coma, and nacrolepsy.
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PMID:Workup and management of patients with syncope. 767 89

It is known that the antimalarial drug mefloquine may cause neurological side-effects. Only few cases of encephalitis ascribed to mefloquine treatment have been reported. We here describe a 34 year-old female patient with symptoms of acute brain syndrome. The patient was initially treated with mefloquine for infection with P. falciparum. She was rehospitalized 12 days after mefloquine treatment with fever, nausea, dizziness and headache. Her condition worsened and her temperature rose and 15 days after treatment she had generalized convulsions and went into a coma. The EEG was severely abnormal. The patient was discharged 37 days after mefloquine treatment, but it was two months before the EEG was normal and the patient in her usual condition.
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PMID:[Acute brain syndrome after mefloquine treatment]. 799 50

Four patients showing classic physical stigmata of traumatic asphyxia were studied. Cervicofacial cyanosis and edema, subconjunctival hemorrhage, and multiple ecchymotic hemorrhage of the face, neck, and upper part of the chest were documented. Admission Glasgow coma scale scores ranged from 8 to 15. All but one had no associated injury. Skin discoloration resolved within 3 weeks. Complete resolution of subconjunctival hemorrhage occurred 1 month later. In our series, sore throat, hoarseness, dizziness, numbness, and headaches were common. Profound lower leg pitting edema, hemoptysis, hemotympanum, and transient visual loss were noted. Chest radiographic findings were normal in all patients. Microscopic hematuria was noted in one patient. Diagnosis is made from the history and characteristic appearance of the patient. Treatment is directed to the associated injury. Oxygen supplement with head elevation to 30 degrees is the mainstay of treatment. If the patient survives the initial insult, the prognosis is excellent.
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PMID:Traumatic asphyxia. 813 32

Neuroendocrine pancreatic tumors are neoplasms derived from APUD cells, characterized by hyperincretion of several peptides of hormonal activity. The incidence of these tumor is low. They are usually classified according to the predominant secreted peptide: gastrinoma, insulinoma, VIPoma, glucagonoma. Insulinoma is the most frequent endocrine pancreatic tumor, characterized by a peculiar clinical picture due to insulin action. This neoplasm is prevalently benign (90%), and may cause symptoms due to hypo-glycemia such as epilepsy, asthenia, deep coma, dizziness, hunger and epigastric pain. Surgery still constitutes the principal therapy for insulinoma treatment, but an accurate tumor identification is necessary. Selective arteriography of the pancreas and new diagnostic investigations as intraoperative US, selective sampling of pancreatic veins with insulin Quick-RIA, aid the diagnosis and more precise localization of the tumor. When surgical therapy is not practicable, for diffuse metastases, octreotide has an inhibitory effect upon hormone release, and may be combined with chemotherapy for controlling clinical symptoms. We review the clinical records of 2 patients from our Institute, who had hyper-insulinism due to benign insulinomas of the tail of the pancreas. Surgical treatment was performed with enucleation of the neoplasms.
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PMID:[Pancreatic insulinomas]. 817 52

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

The authors studied 24 patients with a Glasgow Coma Scale score of 14 or 15 and normal computerized tomography scans after minor head injury. The study protocol included obtaining serial measurements of S-100 protein in serum during the first 12 hours after injury and early magnetic resonance (MR) imaging. Four patients (17%) had detectable levels of S-100 protein in serum. The S-100 protein levels were highest immediately after trauma, declining hour by hour. In two patients, MR imaging revealed intracranial contusion. Levels of S-100 protein were not detectable in serum in one patient with MR-verified cerebral contusion, but the first measurements were made late, 6 hours after trauma. The highest serum level of S-100 protein (0.9 microgram/L) was seen in a 73-year-old man 2 hours after injury. Magnetic resonance imaging revealed a contusion of the left cerebellar hemisphere, and the patient suffered permanent sequelae of impaired posture and dizziness.
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PMID:Serial S-100 protein serum measurements related to early magnetic resonance imaging after minor head injury. Case report. 889 37

The etiology of sympathotonic orthostatic hypotension (SOH) is still unknown. We reported a 50-year-old male case of SOH associated with herpes simplex encephalitis. Eight days before admission to our hospital, he noticed fever, which was followed by intractable hiccup. He was admitted to a local hospital, where nuchal rigidity and mononuclear CSF pleocytosis were noted. On the 9th hospital day, he suddenly developed respiratory arrest, and his consciousness state deteriorated to coma. He was transferred to our hospital with artificial ventilation on the same day. The second CSF examination revealed pleocytosis and positive herpes-simplex-virus antibody. CAT scan showed diffuse high density areas in the bilateral temporal lobes. Intensive anti-herpetic therapy was started. On the 14th hospital day, spontaneous respiration came back and consciousness state was improved from coma to stupor. He gradually recovered to alert state and became ambulatory by the 30th hospital day. Seven weeks after the onset of his illness, he noticed orthostatic dizziness for the first time during his rehabilitation exercises. Blood pressure was 116/78mmHg at supine position and 82/62mmHg at standing position, and the heart rate was 83bpm, and 141bpm, respectively. Plasma noradrenaline concentration was 0.09 ng/ml (within normal range) at supine position, but increased to 0.29ng/ml upon standing. Catecholamine infusion tests revealed hyposensitivity in beta 2-receptors; decrease in blood pressure in response to isoprenaline was blunted, while increase of blood pressure to noradrenaline was not impaired. Nerve conduction studies and sweating tests were normal. When he was discharged from our hospital on the 87th hospital day, he still had orthostatic symptoms. His complete recovery took full one year. Some authors claimed that SOH is an abortive form of acute autonomic neuropathy, while others postulated that it was due to unbalanced cardiovascular alpha- and beta-adrenoceptor functions. SOH of the present case seems to be caused by the central nervous lesions; especially, the brain stem involvement due to herpes simplex encephalitis may well be causing SOH.
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PMID:[A case of sympathotonic orthostatic hypotension following herpes simplex encephalitis]. 899 41

Syncope is a common phenomenon, well-known to all pediatricians: it is defined as a sudden transient loss of consciousness associated with inability to maintain postural tone that is incompatible with a seizure disorder, vertigo, dizziness, coma, shock or other states of altered consciousness. The purpose of this study are to analyse the multiple causes of syncope, to determine the characteristics of pediatric patients with syncope, to define the pathophysiologic mechanisms that result in neurally mediated syncope.
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PMID:[Syncopal pathology in childhood (I)]. 934 Jun 6


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