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)

Despite therapeutic treatment with lithium or valproate, patients with bipolar I disorder often require adjunctive therapy to treat persistent symptoms. In order to evaluate the effects of quetiapine for bipolar symptoms inadequately responsive to mood stabilizers, a retrospective chart review was undertaken at the Veterans Affairs (VA) Long Beach Mood Disorders Clinic for all bipolar I outpatients who had been prescribed adjunctive quetiapine during an 18-month study period. Among 75 lithium- or valproate-treated patients receiving quetiapine, 16 were identified in whom therapeutic treatment with lithium (> or =0.8 meq/l) or valproate (> or =75 microg/ml) could be verified during the 2-month period prior to quetiapine initiation. Chart notes were utilized by the principal investigator to assign Clinical Global Impression Bipolar ratings (CGI-BP) before and after 30-120 days of quetiapine treatment (mean=173+/-157 mg). Nine of 16 lithium- or valproate-stabilized bipolar patients (56%) were judged much or very much improved in CGI-BP overall ratings following adjunctive quetiapine. In addition, for the entire sample, quetiapine augmentation resulted in significant improvements in clinician-rated bipolar severity scores (CGI-BP) for mania, depression, and overall bipolar illness. The majority of quetiapine-related symptomatic improvement was due to diminished insomnia, agitation, irritability, and mood disturbance. Side effects were mild and transitory including sedation and dizziness. Low-dose quetiapine may be a useful and well-tolerated adjunct for some bipolar patients with incomplete response to lithium or valproate.
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PMID:Adjunctive quetiapine in bipolar patients partially responsive to lithium or valproate. 1292 20

An altered glutamatergic transmission within the central nervous system is supposed to be involved in the generation and propagation of neuropathic pain. Results from experimental studies with animal models of neuropathic pain demonstrate that glutamate antagonists have a positive effect on various parameters. Clinical studies with the NMDA-receptor antagonists ketamine, amantadine, memantine and dextromethorphan and with the antiepileptics gabapentin and lamotrigine, which reduce presynaptic release of glutamate,have been performed. They have shown that most of these substances can reduce neuropathic pain. Important side effects of the NMDA receptor antagonists are hallucination and agitation, whereas tiredness and dizziness are the ones of the antiepileptics. Till now, glutamate antagonists are not drugs of first choice for the treatment of neuropathic pain. However, they are an effective alternative in case the established drugs are not helpful or are not tolerated well.
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PMID:[Glutamate antagonists for treatment of neuropathic pain]. 1292 75

(1) Lithium is the first-line treatment for patients with acute mania. For patients with psychosis or intense agitation, an oral neuroleptic can be added (haloperidol or chlorpromazine, the best-assessed drugs of this class). (2) The licensed indications for oral olanzapine, a neuroleptic, explicitly mention the treatment of acute mania. (3) The clinical evaluation dossier on olanzapine in this setting (10 mg to 15 mg/day) is not particularly impressive. In particular, clinical trials included patients with a variety of associated psychotic symptoms. (4) The only comparative trial against another neuroleptic, haloperidol at a high starting dose (10 mg), showed that olanzapine was no more effective. The same applies to a trial comparing olanzapine with disodium valproate. (5) One placebo-controlled trial tested olanzapine as an additional treatment in patients who did not respond adequately to lithium or valproate disodium. Olanzapine potentiated the antimanic effects of the original treatment but also increased the incidence of adverse effects. (6) In patients with acute mania, the main adverse effects of olanzapine are drowsiness, weight gain, dizziness, and dry mouth. In the trial comparing olanzapine with haloperidol, olanzapine caused fewer extrapyramidal side effects but more weight gain than haloperidol. (7) Olanzapine costs 20 times more than haloperidol in France. (8) In practice, olanzapine is just another neuroleptic approved for the treatment of acute mania in patients with psychotic symptoms and agitation. There is no evidence that olanzapine has the best risk-benefit ratio in this category.
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PMID:Olanzapine: new indication. New indication in acute mania: just another neuroleptic. 1514 54

A cross-sectional study performed in Temeke District (Dar es Salaam, Tanzania) showed that 5.5% of the traditional healers have knowledge for the treatment of epilepsy. Of the 100 healers interviewed, 30 (30%) believed that epilepsy was caused by witchcraft, while 19 (19%) thought epilepsy has a genetic origin which can be inherited. Other healers thought epilepsy can be caused by head injury or malaria (24%), and the remaining 27% did not know the cause. Most of the healers (92%) could present an accurate account on the symptoms of the disease, including dizziness, loss of consciousness, abrupt falling down, frothing from the mouth, loss of memory, biting of the tongue, confusion, and restlessness. They showed competence in the treatment of the disease, whereby 60 plants that are commonly used were mentioned. Abrus precatorius L. (Leguminosae), Clausena anisata (Willd.) Oliv. (Rutaceae) and Hoslundia opposita Vahl (Lamiaceae), which are among the plants mentioned, have proven anticonvulsant activity, while a few other species on their list have been reported to be useful in the treatment of epilepsy. Biological testing of these plants, using different models of convulsions is, suggested.
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PMID:Plants used to treat epilepsy by Tanzanian traditional healers. 1570 73

To thoroughly investigate the phenomenon of atypical antipsychotic associated weight gain, a feeding laboratory paradigm was developed. This study is a randomized, double-blind, parallel group trial comparing the tolerability and effects of a two-week exposure to olanzapine, risperidone or placebo on weight, resting energy expenditure (REE), and eating behaviors in 48 healthy human subjects. Subjects were randomized to receive olanzapine, risperidone, or placebo and titrated over four days to 10 mg/d, or 4 mg/d, respectively. The mean dose at endpoint was 8.75 mg/day for the olanzapine group and 2.88 mg/d risperidone group. Weight changes were significantly different between groups at midpoint (F = 5.477, df = 2, 44, P = .0001). The olanzapine group demonstrated a significant increase in weight at midpoint (1.59 + 1.80 kg, P = .002) and endpoint (2.25 + 1.62 kg, P = .0001) compared to placebo and at endpoint compared to risperidone (1.05 + 1.15 kg, P = .015). Resting energy expenditures corrected for fat free mass did not reveal any differences between groups. Olanzapine subjects demonstrated significantly more dry mouth and sedation versus placebo while risperidone subjects experienced significantly more sedation, dry mouth, dizziness stuffy nose and restlessness than placebo and more dizziness and stuffy nose versus olanzapine subjects. Thus, a human feeding lab paradigm utilizing a brief exposure to atypical antipsychotics functions as a method to investigate pharmacologically induced weight gain.
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PMID:A comparison of the effects of olanzapine and risperidone versus placebo on eating behaviors. 1616 Jun 15

Levetiracetam is a novel antiepileptic drug that has been demonstrated as being effective in the management of partial seizures. It is rapidly and completely absorbed after oral administration and it is predominantly eliminated as unchanged drug in the urine. Its metabolism is independent of the cytochrome P450 enzyme system, nor does it induce cytochrome P450 enzymes. As a result of its pharmacokinetic features, levetiracetam has not been demonstrated to interact with other drugs in either direction. In double-blind, placebo-controlled trials, all the levetiracetam dosages tested were effective, including 1000 mg/day, 2000 mg/day and 3000 mg/day. The ineffective dose is not known. Efficacy seemed to be maintained in long-term studies, with no evidence of tolerance. In major double-blind, placebo-controlled trials discontinuation rates because of adverse events were 6.9-10.9% for levetiracetam-treated patients (all doses) compared with 5.3-8.6% for placebo-treated patients. The most common adverse events that differed between treatment groups and placebo control groups were somnolence, asthenia, dizziness and, in the US study, infection. Since levetiracetam was marketed, behavioural effects have been reported, namely irritability, agitation, anger and aggressive behaviour. These adverse effects are more likely in learning disabled individuals, those with prior psychiatric history and those with symptomatic generalised epilepsy. Overall, the risk has been estimated at 12-15%. Laboratory parameters overall seem to be not significantly affected by levetiracetam, although slight trends to lower white and red blood cell counts were detected in the studies. No organ toxicity has been described so far, with patient exposures exceeding 500,000. In summary, levetiracetam exhibits a very favourable safety profile in patients with partial onset seizures. Whereas somnolence, asthenia and dizziness were the most prominent adverse effects in clinical trials, behavioural adverse effects have generally been the most common reason for drug discontinuation in clinical practice.
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PMID:Benefit-risk assessment of levetiracetam in the treatment of partial seizures. 1618 Sep 37

Acute agitation is a common psychiatric emergency often treated with intramuscular (i.m.) medication when rapid control is necessary or the patient refuses to take an oral agent. Conventional i.m. antipsychotics are associated with side effects, particularly movement disorders, that may alarm patients and render them unreceptive to taking these medications again. Ziprasidone (Geodon) is the first second-generation, or atypical, antipsychotic to become available in an i.m. formulation. Ziprasidone IM was approved by the Food and Drug Administration in 2002 for the treatment of agitation in patients with schizophrenia. In October 2004, a roundtable panel of physicians with extensive experience in the management of acutely agitated patients met to review the first 2 years of experience with this agent. This monograph, a product of that meeting, discusses clinical experience to date with ziprasidone IM and offers recommendations on its use in various settings. In clinical trials, patients treated with ziprasidone IM demonstrated significant and rapid (within 15-30 minutes) reduction in agitation and improvement in psychotic symptoms, agitation, and hostility to an extent greater than or equal to that attained with haloperidol i.m. Tolerability of ziprasidone IM was superior to that of haloperidol IM, with a lower burden of movement disorders. Clinical trials have also shown that ziprasidone IM can be administered with benzodiazepines without adverse consequences. Transition from i.m. to oral ziprasidone has been well tolerated, with maintenance of symptom control. The most common adverse events associated with ziprasidone IM were insomnia, headache, and dizziness in fixed-dose trials and insomnia and hypertension in flexible-dose trials. No consistent pattern of escalating incidence of adverse events with escalating ziprasidone doses has been observed. Changes in QTc interval associated with ziprasidone at peak serum concentrations are modest and comparable to those seen with haloperidol IM. Results of randomized clinical trials of ziprasidone IM have been corroborated in studies in real-world treatment settings involving patients with extreme agitation or a recent history of alcohol or substance abuse. In these circumstances, clinically significant improvement was seen within 30 minutes of ziprasidone IM administration, without regard to the suspected underlying etiology of agitation. Agents with a good safety/tolerability profile, such as ziprasidone IM, may be more cost effective long term than older agents, due to reduced incidence of acute adverse effects (eg, acute dystonia) that often require extended periods of observation. Additional trials of ziprasidone IM in agitated patients in a variety of clinical setting are warranted to generate comparative risk/benefit data with conventional agents and other second-generation antipsychotics.
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PMID:Best clinical practice with ziprasidone IM: update after 2 years of experience. 1624 23

Published literature on the toxicity of a topiramate overdose is limited to case reports. This retrospective study of poison center data was performed to examine the severity of topiramate overdoses. Data on single substance exposures to topiramate reported to the American Association of Poison Control Centers (AAPCC) Toxic Exposure Surveillance System (TESS) in 2000 and 2001 were retrospectively analysed. A total of 567 cases met the inclusion criteria, of which 39% occurred in adults over 19 years of age and 30.2% in children < or = 4 years old. The majority of patients (62.1%) experienced no toxicity. The most common clinical effects reported were drowsiness/lethargy (15.5%), dizziness/vertigo (4.9%), agitation (4.9%), confusion (3.9%), nausea (2.6%) and vomiting (2.5%). Symptomatic patients were older than asymptomatic patients and adults were more likely to be managed in a healthcare facility (P <0.0001). Patients who received gastrointestinal decontamination experienced less serious outcomes than those without decontamination (P <0.02). It is concluded that clinicians should expect relatively mild mental status changes in adults or children with toxicity from topiramate overdose. Serious toxic effects, such as CNS depression with respiratory depression or persistent non-anion gap metabolic acidosis, are infrequent.
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PMID:Evaluation of toxicity of topiramate exposures reported to poison centers. 1632 76

This article updates a 1990 review of the effects of tobacco abstinence by reviewing (a) which symptoms are valid indicators of tobacco abstinence and (b) the time course of tobacco abstinence symptoms. The author searched several databases to locate more than 3,500 citations on tobacco abstinence effects between 1990 and 2004; 120 of these were used in this review. Data collection and interpretation were based solely on the author's subjective judgments. For brevity, the review does not evaluate craving, hunger, performance, and several other possible outcomes as withdrawal symptoms. Anger, anxiety, depression, difficulty concentrating, impatience, insomnia, and restlessness are valid withdrawal symptoms that peak within the first week and last 2-4 weeks. Constipation, cough, dizziness, increased dreaming, and mouth ulcers may be abstinence effects. Drowsiness, fatigue, and several physical symptoms are not abstinence effects. In conclusion, no major changes are suggested for DSM-IV criteria for tobacco/nicotine withdrawal, but some deletions are suggested for ICD-10 criteria. Future studies need to investigate several possible new symptoms of withdrawal and to define more clearly the time course of symptoms.
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PMID:Effects of abstinence from tobacco: valid symptoms and time course. 1736 63

The characteristics of disturbing primary headache and the occurrence of headache types were studied by sending a questionnaire to 1132 Finnish families of 6-year-old children. Children with headache in the preceding 6 months and their controls were clinically examined at the ages of 6 and 13. During the follow-up, half of the headaches, classified as migraine at age 6 years, were unchanged and 32% turned into tension-type headache. In children with tension-type headache, the situation was unchanged in 35%, and in 38% of children the headache type had changed to migraine. At preschool age the most common location of headache was bilateral and supraorbital, and at puberty bilateral and temporal. During the follow-up, symptoms concurrent with headache, such as odour phobia, dizziness and balance disturbances became more typical, whereas restlessness, flushing and abdominal symptoms became less marked. The early manifestation of both migraine and tension-type headache predict equally often migraine in puberty with marked changes in concurrent symptoms and pain localization.
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PMID:Changing headache from preschool age to puberty. A controlled study. 1737 6


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