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)

Oxycodone is a semi-synthetic opioid with an agonist activity on mu, kappa and delta receptors. Equivalence with regard to morphine is 1:2. Its effect commences one hour after administration and lasts for 12 h in the controlled-release formulation. Plasma halflife is 3-5 h (half that of morphine) and stable plasma levels are reached within 24 h (2-7 days for morphine). Oral bioavailability ranges from 60 to 87%, and plasma protein binding is 45%. Most of the drug is metabolised in the liver, while the rest is excreted by the kidney along with its metabolites. The two main metabolites are oxymorphone--which is also a very potent analgesic--and noroxycodone, a weak analgesic. Oxycodone metabolism is more predictable than that of morphine, and therefore titration is easier. Oxycodone has the same mechanism of action as other opioids: binding to a receptor, inhibition of adenylyl-cyclase and hyperpolarisation of neurons, and decreased excitability. These mechanisms also play a part in the onset of dependence and tolerance. The clinical efficacy of oxycodone is similar to that of morphine, with a ratio of 1/1.5-2 for the treatment of cancer pain. Long-term administration may be associated with less toxicity in comparison with morphine. In the future, both opioids could be used simultaneously at low doses to reduce toxicity. It does not appear that there are any differences between immediate and slow-release oxycodone, except their half-life is 3-4 h, and 12 h, respectively. In Spain, controlled-release oxycodone (OxyContin) is marketed as 10-, 20-, 40- or 80-mg tablets for b.i.d. administration. Tablets must be taken whole and must not be broken, chewed or crushed. There is no food interference. The initial dose is 10 mg b.i.d. for new treatments and no dose reduction is needed in the elderly or in cases of moderate hepatic or renal failure. Immediate-release oxycodone (OxyNorm) is also available in capsules and oral solution. Side effects are those common to opioids: mainly nausea, constipation and drowsiness. Vomiting, pruritus and dizziness are less common. The intensity of these side effects tends to decrease over the course of time. Oxycodone causes somewhat less nausea, hallucinations and pruritus than morphine.
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PMID:Oxycodone: a pharmacological and clinical review. 1752 40

Bajiaolian (Dysosma pleianthum), a species in the Mayapple family (Podophyllum pelatum), has been widely used as a traditional Chinese herbal medication for the remedies of snake bite, tumor growth, post-partum recovery, and acne. It has also been used in western medicine, especially topically for various skin lesions. Both oral ingestion and dermal application may result in severe toxicity. The clinical presentations reported after Bajiaolian poisoning include nausea, vomiting, diarrhea, abdominal cramps, tachycardia, orthostatic hypotension, paralytic ileus, urinary retention, hepatorenal dysfunction, leukocytosis followed by leukopenia, thrombocytopenia, prolonged areflexia, prolonged paraethesia and sensory ataxia, dizziness, fever, memory impairment, hallucinations, paranoia, convulsion, fainting, and coma. There are no previous reports in the literature about the cessation of nail growth as a clinical presentation following Bajiaolian poisoning. We present a case of nail growth that was halted for more than seven years after a single case of Bajiaolian poisoning.
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PMID:Cessation of nail growth following Bajiaolian intoxication. 1785 56

Our objective was to perform a meta-analysis of randomized controlled trials of dopamine agonists (DA) as monotherapy as well as adjunctive therapy for the early treatment of Parkinson's disease (PD). A systematic literature search was conducted through April 2007. Both efficacy and safety endpoints were evaluated. DA monotherapy showed superior efficacy but more frequent adverse events compared to placebo. In addition, DA demonstrated inferior efficacy to levodopa, but was associated with fewer motor complications. However, DAs were associated with a greater incidence of nuisance side effects, such as hallucinations, somnolence and dizziness. The use of DA is an effective treatment option for the treatment of early PD and appears especially useful among PD patients with wearing-off phenomenon or dyskinesias on levodopa; however it may result in more adverse events and higher withdrawal rates.
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PMID:Dopamine agonists in the treatment of early Parkinson's disease: a meta-analysis. 1877 43

Ropinirole prolonged release is a once-daily, 24-hour formulation of ropinirole, a non-ergot dopamine agonist. It is approved as monotherapy and as an adjunct to levodopa in the treatment of Parkinson's disease (PD). Several potential advantages of ropinirole prolonged release compared to the immediate release formulation include maintaining more consistent dopaminergic activity with steadier plasma levels, increased tolerability, greater compliance from a simpler once-daily dosing regimen and ease in dose titration. In a randomized, double-blind, non-inferiority, crossover study, ropinirole prolonged release was shown to have comparable efficacy and tolerability to immediate release ropinirole in early PD patients, with significantly greater compliance. Subjects were converted overnight between ropinirole formulations without loss of efficacy and with good tolerability. In a randomized, double-blind, placebo-controlled study in advanced PD, daily "off" time was reduced by an average of 2.1 hours with ropinirole prolonged release compared to 0.4 hours with placebo. Patients on ropinirole prolonged release were also more likely to require less daily levodopa. Ropinirole prolonged release is well tolerated with a similar adverse effect profile to other non-ergot dopamine agonists. The most common adverse effects include dyskinesia, nausea, dizziness, hallucinations, somnolence, abdominal pain or discomfort and orthostatic hypotension. Ropinirole prolonged release is a safe and effective treatment option for both early and advanced PD. This manuscript briefly reviews the current pharmacological treatment options for PD and provides a more detailed review of the currently available data regarding ropinirole prolonged release as a treatment option for PD.
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PMID:A review of ropinirole prolonged release in Parkinson's disease. 1950 79

(1) When oral morphine does not relieve severe pain and when there is no specific treatment for the underlying cause, the first option is to try subcutaneous or intravenous administration. If this standard treatment fails or is poorly tolerated, intrathecal injection is usually preferred as the direct route to the central nervous system. However, one-quarter to one-half of patients still do not achieve adequate pain relief, and adverse effects are relatively frequent; (2) Ziconotide is not an opiate and is not related to the usual classes of drugs that interfere with nervous transmission in the posterior horn of the spinal cord. Marketing authorization has been granted for "severe, chronic pain in patients who require intrathecal analgesia". The Summary of Product Characteristics (SPC) recommends continuous infusion via an intrathecal catheter connected to a pump; (3) Clinical evaluation of ziconotide does not include any trials versus morphine in patients with nociceptive pain, or any trials versus tricyclic or antiepileptic drugs in patients with neurogenic pain; (4) In a trial in 220 patients in whom systemic morphine had failed, the mean pain score on a 100-mm visual analogue scale was 69.8 mm after three weeks on ziconotide, compared to 75.8 mm with placebo. This difference, although statistically significant, is clinically irrelevant. The proportion of "responders" (reduction of at least 30% in the initial pain score) was respectively 16.1% and 12.0% (no statistically significant difference); (5) The two other placebo-controlled trials included 112 patients with pain linked to cancer or HIV infection, and 257 patients with non-cancer pain. After a titration phase lasting 5 to 6 days, a combined analysis of the two trials showed that the mean pain score was 48.8 mm with ziconotide and 68.4 mm with placebo (statistically significant difference). However, many patients did not complete the titration phase. Efficacy also appeared to differ according to the type of pain; ziconotide was more effective on cancer pain than on neurogenic pain; (6) The main adverse effects of ziconotide in clinical trials were cerebellovestibular disorders such as ataxia, dizziness, and gait disorders, as well as confusion, hallucinations (increased in cases of overdose), nausea, vomiting, postural hypotension, and urine retention. About 40% of patients had an elevation in muscle creatine kinase activity, through an unknown mechanism; (7) Intrathecal administration carries a risk of infection (especially meningitis). Some patients might experience a paradoxical increase in pain with ziconotide; (8) In practice, the efficacy of ziconotide in relieving neurogenic pain remains to be established. In cancer pain, the available evidence showing that ziconotide is effective after opiate failure is too weak in view of the potential risks. It is better to re-examine and, if possible, correct the reasons for opiate treatment failure rather than prescribe ziconotide.
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PMID:Ziconotide: new drug. Limited analgesic efficacy, too many adverse effects. 1953 Mar 73

Multiple sclerosis, is an idiopathic inflammatory disease of the central nervous system. Symptoms rarely begin before age 10 or after age 60.The presentation may vary from isolated motor or sensory impairment to seizures or psychotic disturbances. This case report presents a 7-year-old male who complained of double vision, paralysis of the right face and imbalance. At that time the patient had supranuclear facial palsy, mild ataxia, diplopia and horizontal nystagmus. Head CT scan showed nodular densities with low attenuation areas in the white matter of the left frontal and left parietal lobes compatible with multiple sclerosis. At 12 years of age the patient presented dizziness, diplopia, and weakness of right extremities. At 24 years of age he developed seizures and visual and auditory hallucinations. By age 28 the patient was admitted with a sudden onset of paraparesis. Extensive subcortical and periventricular white matter changes were demonstrated by MRI on February 7, 2004. This case, with symptoms beginning at a very young age, demonstrates a wide range of the presentations of multiple sclerosis: motor impairments, seizures and hallucinations.
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PMID:Multiple sclerosis originating in childhood associated with seizures and hallucinations. 1961 May 59

A wide range of drugs can cause mental status changes. Fluoroquinolones are one among them and are underrecognised.The CNS side effects of levofloxacin like headache, dizziness, restlessness, tremor, insomnia, hallucinations, convulsions, anxiety and depression are well documented. We report a rare case of middle aged diabetic male admitted to hospital with multiple infections who developed acute psychosis following levofloxacin administration.
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PMID:Levofloxacin-induced acute psychosis. 1977 10

Zolpidem is a short-acting nonbenzodiazepine hypnotic used for the treatment of insomnia. It works quickly and has a short half-life of 2-3 h. Significant side effects are reported including dizziness, amnesia, and even hallucinations. In this method, zolpidem is extracted from blood or other biological fluids/tissues using solid phase extraction technology for analysis. The extract is then assayed using selected ion monitoring gas chromatography/mass spectrometry for absolute confirmation of the compound. The quantitation of this drug is made from standard curves constructed using selected ion monitoring and peak-area ratios of analyte vs. internal standard of quantifying ions.
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PMID:Identification and quantitation of zolpidem in biological matrices using gas chromatography-mass spectrometry (GC-MS). 2007 4

Parkinson disease (PD) is a chronic progressive degenerative disorder that affects over 6 million people worldwide. It is manifested by motor and psychiatric signs. The latter inflicts up to 88% of PD patients. With the prolongation of life expectancy, it is presumed that the prevalence of PD will further rise, together with comorbid depression. As a result, the need for an adequate therapeutic answer for compounded PD with depression is called for urgently. Several theories try to explain the trigger of depression in PD patients by impaired activity in dopamine, norepinephrine and serotonin systems. Various treatment to combat depressive symptoms in PD patients were proposed and are in use, with ambiguous results and disturbing side effects. These anti-depressive modalities include SSRI's, SNRI, TCA, NRI and ECT. Dopamine agonists showed some anti-depressant activity in several studies in depressive PD, but may cause side effects such as dizziness, somnolence, confusion and even hallucinations. The role of dopamine agonists in the treatment of depression is still being explored because of no sufficient number of controlled studies in this area. Our hypothesis is to suggest NDRI - Bupropion - as the first line of treatment in PD patients with depression, in PD induced depression and/or in depression triggered by one of the treatments given for PD. Dual norepinephrine and dopamine reuptake inhibition is associated with unique clinical profile that compounds together anti-depressant efficacy without serotonin associated side effects such as weight gain, sedation, sexual dysfunction. Bupropion, as mainly dopaminergic and noradrenergic anti-depressant can alleviate therapeutically depressive symptoms associated with PD. Clinical controlled studies on Bupropion use in PD depressed patients are required to support this hypothesis.
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PMID:Bupropion as the treatment of choice in depression associated with Parkinson's disease and it's various treatments. 2070 40

Vertigo can be defined as an illusion or hallucination of movement. The control of balance is complicated. Vertigo can be caused by many different pathologies, some of which are potentially life threatening. An important differentiation is whether the symptoms of vertigo originate from a central or peripheral origin. Clues to a central origin are other brainstem symptoms or signs of acute onset such as headache, deafness and other neurological findings. These patients warrant urgent referral and investigation. Red flags in patients with vertigo include: headache; neurological symptoms; and neurological signs. It is useful to categorise vertigo into acute and chronic. The former usually has a single mechanism whereas chronic dizziness is often multifactorial. History is usually the most important part of the assessment. Key questions should be asked and it is vital to establish if the patient is suffering from vertigo or some other complaint such as anxiety or syncope. A neurological and otological examination should be performed, appropriate to the history. Assessment of gait and posture is crucial. If the patient has positional vertigo then a Hallpike test should be performed. Visual acuity should be checked as vision is a vital part of the balance system. The cranial nerves should be tested in particular eye movements for any ophthalmoplegia pointing to focal cranial nerve pathology and for nystagmus. The rest of the neurological examination should exclude evidence of central disease, in particular cerebellar disease, and neuropathy. If syncope is suspected it is wise to perform an extensive systemic examination in particular lying and standing BP, and cardiovascular and respiratory system assessments.
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PMID:Systematic approach needed to establish cause of vertigo. 2151 May 8


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