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 apparent case of carbamazepine-induced leukocytosis in a 26-year-old woman is presented. When admitted for psychiatric evaluation, the patient had been receiving carbamazepine for seizures for some time. A hemogram revealed a white blood cell (WBC) count of 21.2 x 10(3)/cu mm. Five days after the patient's medication was changed from carbamazepine (600 mg/day) to phenytoin (400 mg/day) and phenobarbital (120 mg/day), her WBC count was within normal range. When she experienced dizziness and ataxia, the phenytoin and phenobarbital were replaced with carbamazepine (600 mg/day). WBC counts performed 11 and 13 days after resumption of carbamazepine therapy again were significantly elevated. Other drugs administered during hospitalization included chlorpromazine, acetaminophen, and codeine. The possible causes of and pathophysiology of leukocytosis are reviewed. The changes in WBC that occurred with the rechallenge of carbamazepine indicate that the drug was the probable cause of the leukocytosis.
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PMID:Carbamazepine-induced leukocytosis. 737 19

Spirogermanium is a new azaspirane antitumor agent, with the metal germanium substituted for a one-carbon moiety in the ring structure. This drug inhibits DNA and RNA synthesis in HeLa cells, is cytotoxic in vitro, and has curative in vivo antitumor activity against the ascitic Walker 256 carcinosarcoma in rats. No hematologic toxicity was recorded during the preclinical toxicologic evaluation. The principal clinical toxic effects observed in this phase I trial were neurologic, manifested as lethargy, dizziness, and ataxia, while a grand mal seizure was produced after an accidental overdose. There was no evidence of hematologic, renal, or hepatic toxicity. A partial response was achieved in a patient with a well-differentiated lymphocytic lymphoma. We recommend that phase II trials be conducted with a twice or thrice weekly dose of 50-80 mg/m2, administered in a 30-minute iv infusion.
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PMID:Phase I clinical trial of spirogermanium. 745 90

When divers are exposed to extreme atmospheric pressures they may exhibit symptoms of the high pressure nervous syndrome (HPNS). Although clinical HPNS symptoms are well described, little is known about the underlying pathophysiologic mechanisms. Special HPNS signs like vertigo and tremor suggested sensory-motor hyperexcitability resulting from brainstem dysfunction. We therefore studied brainstem auditory evoked potential (BAEP) repeatedly in four divers during an experimental deep helium-oxygen saturation dive to 450 meters of seawater (msw). Wave I (auditory nerve response) latency decreased whereas interpeak latencies (IPLs) I-III and I-V, which indicate respective cochleo-pontine and cochleo-mesencephalic transmission time, prolonged during the dive. IPLs III-V also prolonged the dive, but with greater variability among divers. Two divers showed a marked reversal of the normal attenuation effect of increased stimulus presentation rates on IV and V amplitudes during compression, an effect that subsided during the stay at bottom depth. This finding might indicate a relative enhancement of synaptic excitability and is presumed to be a feature of HPNS. Wave I latency reduction might at least partly be caused by accelerated sound conduction in dense helium. Additionally, an upward shift of middle ear resonance frequencies in helium can induce a basal shift of the main cochlear portion responding to the wide band clicks. This effect may reduce wave I latency due to greater relative input from the basal high frequency-short latency-cochlear neurons. Pressure-induced decrease of nerve conduction velocity, delay of synaptic transmission, and inhibitory modulation of midbrain auditory afferents possibly contributed to observed interpeak latency prolongations. Clinical HPNS signs, such as tiredness, dizziness, postural and intentional hand tremor, ataxia, and opsoclonus, were noted in three divers after reaching 300 msw and continued throughout the 37-h stay at bottom depth.
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PMID:Brainstem auditory evoked potentials during a helium-oxygen saturation dive to 450 meters of seawater. 758 Jul 64

We investigated motion sickness evoked by walking while wearing horizontally reversing goggles. The subjects were 36 healthy adults and 90 children aged 4 to 15 years. Most adults soon displayed not only severe sickness, but also dizziness and instability. Instability was certified by Graybiel's ataxia tests in 10 adults. Young children aged 4 to 5 years rarely became sick; however, they showed marked ataxia manifested as drunken gait, falling, or failure to stand up. In older children, autonomic nervous symptoms became manifest and more severe, but ataxia became less severe since locomotion was stopped by uncomfortable symptoms. The present study strongly suggests that motion sickness makes animals learn loss of spatial orientation, which inevitably produces loss of balance.
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PMID:Teleology of motion sickness. 761 Jul 87

Lamotrigine is an antiepileptic drug which is believed to suppress seizures by inhibiting the release of excitatory neurotransmitters. Efficacy has been demonstrated for lamotrigine as add-on therapy to existing regimens in patients with resistant partial seizures. Total seizure frequency was reduced by 17 to 59% compared with placebo, and 13 to 67% of patients experienced reductions of > or = 50% in seizure frequency. Secondarily generalised tonic-clonic seizures respond well to lamotrigine, and there is preliminary evidence of improvement in patients with primary generalised seizures, Lennox-Gastaut syndrome and in children with multiple seizure types. Seizure control has been maintained in patients who have continued to receive lamotrigine as monotherapy after discontinuation of other medications. Results of one trial suggest similar efficacy for lamotrigine monotherapy as for carbamazepine, but confirmation of its use in this setting awaits more extensive controlled comparisons with established agents. Adverse events associated with lamotrigine as add-on therapy are typical of antiepileptic drugs, namely dizziness, ataxia and other CNS-related symptoms. Rash, which has occurred in 10% of patients in placebo-controlled trials, may be severe and its appearance has led to discontinuation of therapy in 1% of patients. Lamotrigine appears well tolerated in the longer term, but this facet of its profile requires further monitoring. Influences of valproic acid and enzyme-inducing anti-epileptics on lamotrigine eliminate necessitate dosage modification of lamotrigine. Conversely, lamotrigine has little apparent influence on the pharmacokinetics of other agents, although it may increase plasma concentrations of the active metabolite of carbamazepine during concomitant administration. Thus, lamotrigine permits improved seizure control in some patients with refractory partial seizures, and may prove to be especially effective in secondarily generalised tonic-clonic seizures. As is usual at this stage in a drug's development, several aspects of the profile of lamotrigine are incompletely defined, notably its efficacy in other seizure types, in children, as monotherapy, and its longer term tolerability. Nonetheless, lamotrigine presently offers a worthwhile alternative for the physician confronted with the challenge of treating patients with intractable partial seizures with or without secondarily generalised seizures, and shows potential for broader applications in other areas of epilepsy management.
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PMID:Lamotrigine. A review of its pharmacological properties and clinical efficacy in epilepsy. 769 4

Gabapentin is an antiepileptic drug with an unknown mechanism of action apparently dissimilar to that of other antiepileptic agents, and possessing some desirable pharmacokinetic traits. The drug is not protein bound, is not metabolised and does not induce liver enzymes, diminishing the likelihood of drug interactions with other antiepileptic agents and drugs such as oral contraceptives. Although gabapentin is a structural analogue of the neurotransmitter gamma-aminobutyric acid (GABA), which does not cross the blood-brain barrier, gabapentin penetrates into the CNS and its activity is seemingly distinct from GABA-related effects. Present clinical evaluation is largely restricted to proof of efficacy trials of gabapentin as add-on therapy in patients with partial epilepsy resistant to conventional treatment. Gabapentin (usually 600 to 1800 mg/day) provides notable benefit, reducing seizure frequency by > or = 50% in 18 to 28% of patients with refractory partial seizures, as shown in 3 double-blind, placebo-controlled trials. Overall, seizure frequency decreased by 18 to 32% during 3-month treatment periods. Patients with complex partial seizures, and partial seizures secondarily generalised, are particularly likely to respond to gabapentin. Current experience with the drug in other seizure types, and as monotherapy, is limited. Mild adverse events, commonly somnolence, fatigue, ataxia and dizziness, have been reported in about 75% of gabapentin recipients. While the drug has been well tolerated when administered to a few patients for periods of up to 5 years, its long term tolerability profile has yet to be fully expounded. Thus, with its favourable pharmacokinetic profile, and efficacy in some refractory patients, gabapentin is poised to fill a niche as an adjunct to the treatment of partial epilepsy. Promising results obtained thus far warrant further work to clarify its long term tolerability, its possible efficacy in other seizure types, its position relative to other agents and its use as monotherapy. In the meantime, gabapentin is likely to provide a much-needed option in a therapeutic area requiring complex management.
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PMID:Gabapentin. A review of its pharmacological properties and clinical potential in epilepsy. 769 32

Wolfram's syndrome is defined by the association of diabetes mellitus, diabetes insipidus, optic atrophy and nerve deafness. Other neurological anomalies, such as ataxia, nystagmus, tonic pupil, dizziness, dysarthria, dysphagia and epilepsy are rarely described and tend to appear later than the primary manifestations. We describe a patient with Wolfram's syndrome whose magnetic resonance image (MRI) of the head showed brainstem and cerebellar atrophy years before the appearance of clinical signs of brainstem disfunction. We conclude that alterations in MRI precede neurological symptoms by several years in Wolfram's syndrome.
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PMID:[Wolfram's syndrome: correlation of clinical signs and neurological images]. 769 38

We report open-label clinical observations of additional lamotrigine (LTG) in 16 adult patients with refractory epilepsy, aimed to assess the long-term efficacy and safety of LTG in clinical use. LTG was added to the current antiepileptic drug (AED) regimen at a daily dosage of 200-400 mg depending on the concomitant treatment. Ten patients completed one year's treatment and were followed up to an overall exposure ranging 15-38 months. Six patients (38% of the initial group) had a reduction of seizure frequency greater than 50% of pre-treatment baseline after one year; the further follow-up indicated some efficacy decline, since the percentage of improved patients dropped to 19% after 2 years and 13% after 3 years. The dropouts during the first year were due to seizure breakthrough (two patients), Steven-Johnson-like syndrome (one patient) and reasons unrelated to treatment (three patients); in one patient LTG treatment was stopped due to macrocytic anemia after 23 months. Other reported adverse events were dizziness, mild ataxia, diplopia and localized purpura. No other hematological or biochemical changes were noted. LTG was not associated with any significant changes in plasma concentrations of concomitant AEDs. These findings confirm the moderate efficacy and low toxicity of long-term LTG in severe epilepsy.
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PMID:Long-term observations on the clinical use of lamotrigine as add-on drug in patients with epilepsy. 784 67

As dizziness can be caused by so many different pathophysiological mechanisms, it is crucial to determine the type of dizziness before proceeding with the diagnostic evaluation. Vertigo, defined as an illusion of movement, is an important subtype of dizziness that indicates a lesion somewhere within the vestibular system. Probably the most useful feature for differentiating between peripheral and central causes of vertigo is the associated symptoms. Vertigo of peripheral origin is typically associated with auditory symptoms such as hearing loss and tinnitus, while vertigo of central origin is nearly always associated with neurological symptoms such as diplopia, weakness, numbness and ataxia. Each of the common causes of vertigo has a characteristic clinical profile that should suggest a likely diagnosis after the history and examination are complete. Probably the most important treatment breakthrough is the positional manoeuvre that reliably cures benign positional vertigo (see Chapter 6). The treatment strategy for an acute peripheral vestibular lesion has evolved over the past few years. Patients are encouraged to return to normal physical activity as rapidly as possible. Repeated head, eye and body movements (vestibular rehabilitation) help the brain to recalibrate the relationship between visual, proprioceptive and vestibular signals (Chapter 9).
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PMID:Approach to the dizzy patient. 787 2

Amantadine and rimantadine are recommended for the treatment and prophylaxis of influenza A infections, and constitute an integral component of influenza control measures in the nursing home setting. However, optimal use necessitates a thorough understanding of the toxicity profiles of these agents, as well as strategies to reduce the risk of adverse reactions. Adverse reactions of these compounds predominantly involve the gastrointestinal tract and the central nervous system (CNS), including hyperexcitability, slurred speech, tremors, insomnia, dizziness, mood disturbance, ataxia, psychosis and fatigue. Based on data from comparative trials, rimantadine appears to exhibit a lesser propensity to cause adverse CNS reactions than amantadine, but a similar propensity to cause adverse gastrointestinal reactions. Factors enhancing the risk of adverse reactions to these agents include reduced renal function (especially for amantadine), drug-drug interactions with cationic drugs, which inhibit amantadine renal tubular secretion (e.g. trimethoprim, triamterene, and possibly cimetidine and procainamide), elevated peak and trough plasma concentrations, and a history of seizures. Careful attention to published dosage adjustment guidelines for these compounds, avoidance of interacting drugs and avoiding these agents in patients with a history of seizures may be the best means to reduce the risk of toxicity in elderly patients. Rimantadine may have an advantage over amantadine in the elderly population in light of its lesser propensity to cause adverse reactions, less complex dosage adjustment in the case of renal impairment and probable lack of drug-drug interaction potential with cationic drugs.
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PMID:Amantadine and rimantadine prophylaxis of influenza A in nursing homes. A tolerability perspective. 791 41


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