Prospective, double-blinded, randomised controlled trials (RCTs) investigating the pharmacological treatment of painful HIV-SN with sufficient quality assessed using a modified Jadad scoring method.
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The link between cyclobenzaprine (Flexeril) administration and serotonin syndrome (SS) is subject to debate. Establishing such a connection is difficult because of the limited number of case reports available and the almost complete ignorance of its preclinical pharmacology. In this context, evidence is provided here that cyclobenzaprine blocks the serotonin and norepinephrine transporters and binds to another set of five serotonin receptors. SS should be considered when indicative signs occur in the context of cyclobenzaprine use.
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We included randomised, double-blind studies of at least two weeks duration comparing desipramine with placebo or another active treatment in chronic neuropathic pain. Participants were adults aged 18 years and over. We included only full journal publication articles.
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After CCI surgery, a small magnet was implanted into the operated limb. The rat was placed in a test chamber that was surrounded by wire coil. Limb movements, including lifting/guarding, flinching/shaking, licking and walking in the operated limb, caused changes in the electromagnetic field, including a change in voltage and transformed into a signal via an amplifier.
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An examination of 68 patients with neurotic and psychopathic states detected the existence of significant connections between the method of treatment and reverse development of the symptomatology. The author used sets clinical scales and methods of statistical canonic, regressional and dispersional analysis. The most effective appeared to be autogenic training and aminazine. The effectiveness of aminazine was most distinctly seen in arresting hysterical characterological disturbances. The action of autogenic training in combination with amytriptiline was more effective in the treatment of insomnia and psychopathic disorders of the inhibitive type.
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Warfarin users who initiated citalopram, fluoxetine, paroxetine, amitriptyline, or mirtazapine had an increased risk of hospitalization for gastrointestinal bleeding. However, the elevated risk with mirtazapine suggests that a drug-drug interaction may not have been responsible for all of the observed increased risk.
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There is a legal requirement to provide analgesia for velvet antler removal in New Zealand. Currently, this is achieved using local anaesthetic blockade, with or without systemically administered sedative/analgesic agents, or by compression in 1-year-old stags. Lignocaine hydrochloride 2% is most commonly used and is most effective when administered as a high-dose ring block. Combinations of various amino-amide local anaesthetic agents can achieve rapid onset and prolonged duration of analgesia, though concerns about drug residues and carcinogenic potential of a lignocaine metabolite have led to consideration of the amino-ester family of local anaesthetics as alternatives. Systemically administered analgesics, including opioids, alpha-2-adrenergic agents and ketamine provide dose-dependent sedation and analgesia. However, none are sufficient, alone or in combination, to produce surgical analgesia at currently recommended dose rates and when reversal agents are given, analgesic effects are usually reversed as well as sedation. Thus, local anaesthetic blockade is still indicated, though the potential for drug or drug-metabolite residues in velvet antler remains a concern. The need for and effectiveness of non-steroidal anti-inflammatory drugs (NSAIDs) for post-operative analgesia requires investigation. Amitriptyline, locally administered opioid agonists, tramadol and other systemically administered agents may warrant future investigation for surgical and post-operative analgesia for velvet antler removal.
Fibromyalgia (FM) is still often viewed as a psychosomatic disorder. However, the increased pain sensitivity to stimuli in FM patients is not an "imagined" histrionic phenomena. Pain, which is consistently felt in the musculature, is related to specific abnormalities in the CNS pain matrix. Brain-derived neurotrophic factor (BDNF) is an endogenous protein involved in neuronal survival and synaptic plasticity of the central and peripheral nervous system (CNS and PNS). Several lines of evidence converged to indicate that BDNF also participates in structural and functional plasticity of nociceptive pathways in the CNS and within the dorsal root ganglia and spinal cord. In the latter, release of BDNF appears to modulate or even mediate nociceptive sensory inputs and pain hypersensitivity. We were interested, if BDNF serum concentration may be altered in FM. The present pilot study assessed to our knowledge for the first time BDNF serum concentrations in 41 FM patients in comparison to 45 age-matched healthy controls. Mean serum levels of BDNF in FM patients (19.6 ng/ml; SD 3.1) were significantly increased as compared to healthy controls (16.8 ng/ml; SD 2.7; p<0.0001). In addition, BDNF serum concentrations in FM patients were independent from age, gender, illness duration, preexisting recurrent major depression and antidepressive medication in low doses. In conclusion, the results from our study indicate that BDNF may be involved in the pathophysiology of pain in FM. Nevertheless, how BDNF increases susceptibility to pain is still not known.
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The cured and markedly effective rate was 65.0% (39/60) in the group A, which was superior to 15.9% (10/63) in the group B and 16.1% (9/56) in the group C (both P < 0.001). After treatment, the scores of MPQ and HAMD and the amount of tenderness point all decreased in the three groups, group A being significantly better than group B and group C, and the time of producing effect in the group A was more earlier than those in the group B and the group C.
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Since the last version of this review, the new included studies have not added high quality evidence to support the use of SSRIs or venlafaxine (a SNRI) as preventive drugs for tension-type headache. Over two months of treatment, SSRIs or venlafaxine are no more effective than placebo or amitriptyline in reducing headache frequency in patients with chronic tension-type headache. SSRIs seem to be less effective than tricyclic antidepressants in terms of intake of analgesic medications. Tricyclic antidepressants are associated with more adverse events; however, this did not cause a greater number of withdrawals. No reliable information is available at longer follow-up. Our conclusion is that the use of SSRIs and venlafaxine for the prevention of chronic tension-type headache is not supported by evidence.
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alpha 1-Receptor antagonists and antidepressant agents are basic (cationic) drugs that are known to bind to alpha 1-acid glycoprotein (AAG). Since these drugs are frequently co-administered and since they bind to the same protein, this investigation was designed to evaluate the "in vitro" ability of antidepressants, alpha 1-receptor antagonists, and propranolol to displace [3H]imipramine and [3H]prazosin from the AAG binding site(s). Equilibrium dialysis was employed. Of the drugs studied, the following order of potency in displacing [3H]prazosin was found: trazodone greater than prazosin greater than doxazosin greater than propranolol greater than doxepin = amoxapine = trimazosin = amitriptyline greater than imipramine greater than nortriptyline = desipramine = nomifensine greater than bupropion = maprotiline. [3H]lmipramine binding from AAG was displaced with the following potency order: prazosin greater than imipramine greater than propranolol greater than doxazosin greater than nortriptyline greater than desipramine greater than trimazosin. Tricyclic antidepressants produced similar degrees of displacement of both [3H]imipramine and [3H]prazosin from AAG; whereas, alpha 1-receptor antagonists were more effective displacers of [3H]prazosin than of [3H]imipramine. Furthermore, the demethylated metabolites of imipramine and amitriptyline were less potent displacers than their parent compounds. These results suggest that more than a single binding site may be available for binding to AAG and that hydrophobic bonding is important in the binding of drugs to AAG.
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Twenty patients with HH were examined and interviewed using a standardized questionnaire in regard to their clinical characteristics and effective treatment regimens. Data were evaluated according to current International Headache Society (IHS) diagnostic criteria. Individual treatment history and effective treatment options were compared with expected efficacy based on current literature.
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The degradation rate of amitriptyline hydrochloride in buffered aqueous solution containing various additives was determined. The oxidation was a free radical-mediated process, and the rate was accelerated by the presence of metal-ion contaminants. Glass ampuls, particularly amber ones, in which the solutions were stored were the major source of these contaminants. Edetate disodium stabilized the solution, but the primary antioxidants propyl gallate and hydroquinone were less effective. Sodium metabisulfite accelerated the decomposition, and it is postulated that there was direct attack by metabisulfite at the olefinic double bond in the drug molecule.
No potential interfering peaks were found. Ami and Nor gave rapid elution and baseline resolution. The linear curves of both analyses ranged 0.02-10 nmol and the limit of detection was 0.01 nmol. The recovery (94%-101%) had good precision with relative s of < 8.3%.
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Using isotope technique, the serum binding of amitriptyline (AT), nortriptyline (NT), and quinidine (Q) was measured by equilibrium dialysis in sera containing varying amounts of lipoproteins. Sera were obtained from 10 fasting subjects with normal to grossly elevated levels of cholesterol, triglycerides, or both. When the lipoproteins were removed from eight of the sera by a standard ultracentrifugation technique, the ratio bound/unbound (B/F) AT decreased an average of 47% (range 30% to 68%), NT an average of 54% (range 39% to 67%), and Q an average of 6% (range 0 to 16%). This decrease in the ratio B/F correlated linearly with the sum of serum concentrations of cholesterol and triglycerides for AT (r = 0.88) and NT (r = 0.82), but not for Q (r = 0.15). In three lipoprotein-depleted sera resuspended with lipoproteins at eight different concentrations ranging from 0 to 100% of the original content, there was a linear correlation between the ratio B/F for AT and NT and the lipoproteins, as evidence by cholesterol or triglycerides concentrations (r = 0.97 to 0.99), but not for Q (r = -0.17 to 0.36). Finally, in the original 10 serum samples, there was a linear correlation between the ratio B/F and the serum lipoproteins (sum of cholesterol and triglycerides) for AT (r = 0.89) and NT (r = 0.68), whereas there was no such relationship for Q (r = -0.15). These data indicate that basic drugs differ in binding characteristics (probably depending on lipophility).
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The purpose of this study was to evaluate the patients with acute amitriptyline poisoning and investigate predictive factors for the development of life-threatening complications.
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Carbon monoxide intoxication (COI) can result in severe neuropsychiatric lesions that are however granted little attention in literature. Following the description of affective and neurological symptoms in a 37-year-old female patient five years following COI, we will review, across the literature (Medline 1974--2006), the long-term neuropsychiatric consequences, etiopathogenic hypotheses, prognoses and treatments to apply. Subjective symptoms are reported by the quasi-totality of patients for over more than 30 years following COI. More than half of patients are diagnosed as suffering from cognitive impairments and other neurological symptoms after years following COI. Affective disorders are observed in almost three-fourths of patients and personality disorders in more than half. Numerous cerebral lesions and perfusion disorders can be observed through IRM, PET scan and SPECT and related to the clinical symptomatology of the patient. COI may constitute a risk factor in the waking of long-term neuropsychiatric disorders in a context of environmental and neurobiological complex factor interaction. A close follow-up must be envisaged with neuropsychiatric assessments and regular neuroimagery in order to adapt at best therapeutic interventions to the patient's clinical status. First and foremost prevention and education remain the key solution to the reduction of morbidity and mortality of COI.
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Phantom pain is pain caused by elimination or interruption of sensory nerve impulses by destroying or injuring the sensory nerve fibers after amputation or deafferentation. The reported incidence of phantom limb pain after trauma, injury or peripheral vascular diseases is 60% to 80%. Over half the patients with phantom pain have stump pain as well. Phantom pain can also occur in other parts of the body; it has been described after mastectomies and enucleation of the eye. Most patients with phantom pain have intermittent pain, with intervals that range from 1 day to several weeks. Even intervals of over a year have been reported. The pain often presents itself in the form of attacks that vary in duration from a few seconds to minutes or hours. In most cases, the pain is experienced distally in the missing limb, in places with the most extensive innervation density and cortical representation. Although there are still many questions as to the underlying mechanisms, peripheral as well as central neuronal mechanisms seem to be involved. Conservative therapy consists of drug treatment with amitriptyline, tramadol, carbamazepine, ketamine, or morphine. Based on the available evidence some effect may be expected from drug treatment. When conservative treatment fails, pulsed radiofrequency treatment of the stump neuroma or of the spinal ganglion (DRG) or spinal cord stimulation could be considered (evidence score 0). These treatments should only be applied in a study design.
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The antidepressant efficacy and side-effect profile of amitriptyline were compared to those of moclobemide, a reversible monoamine oxidase inhibitor with selectivity for the type A isozyme. Forty nine patients with DSM-III major depression were randomly assigned to receive either amitriptyline or moclobemide. Thirty seven patients (amitriptyline n = 16, moclobemide n = 21) completed the six week protocol, which was conducted under double blind conditions. The results indicated a comparable antidepressant time course and efficacy for the two treatments. Amitriptyline produced significantly more sedation and antimuscarinic side-effects. Moclobemide appears to be a well tolerated antidepressant without the liability to produce significant postural hypotension and without the need for a tyramine-poor diet.
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Amitriptyline is frequently used to treat patients with interstitial cystitis/painful bladder syndrome. The evidence to support this practice is derived mainly from a small, single site clinical trial and case reports.
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Eighty-six male Wistar rats anesthetized with pentobarbital and mechanically ventilated.
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Untreated serum samples were injected directly into the HPLC system after filtration, leading to be a simple procedure that can be applied in routine analyses for Therapeutic Drug Monitoring.
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Very little is known about antidepressant medication use among First Nations people in Canada. This information would be useful to begin estimating the prevalence of conditions treated with this class of medications and planning appropriate programs. Antidepressant medication claims for First Nations people residing within British Columbia were extracted from the Non-Insured Health Benefits pharmacy database. During 2001, 9.8% (95% CI = 9.81, 9.79) of the population filled a prescription for antidepressant pharmacotherapy, claimant mean age was 40.3 years and the female:male ratio was approximately 3:1. The most common medications were Paxil, Apo-Amitriptyline, Effexor, and Celexa. Use of this medication class is common and more research is needed in this area of study.
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Among 84 women who were randomized, the mean ± standard deviation dose of amitriptyline was 21.7 ± 6.6 mg/day, without statistical difference between the two groups. Pain, as assessed using both the pain rating index of the visual analog scale and the short-form McGill Pain Questionnaire, decreased significantly in both trial groups, with a greater effect seen with the addition of ALA and n-3 PUFAs. The addition of ALA/n-3 PUFAs to amitriptyline treatment was also associated with improvements in dyspareunia and pelvic floor muscle tone. The overall incidence of adverse events was low, and none led to treatment discontinuation.
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Chemotherapy-induced peripheral neuropathy (CIPN) is common among cancer patients who undergo chemotherapy with platinum analogues, taxanes, vinca alkaloids, epothilone, bortezomib, and thalidomide. The purpose of this study was to investigate the evidence of using drugs affecting the central nervous system (CNS) to alleviate CIPN in cancer patients.
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1. Azapirones, selective partial agonists at the 5-HT1A receptor subtype, induce hypothermia and corticotropin (ACTH)/cortisol release as specific functional correlates of central 5-HT1A receptor activation. 2. Compared to controls, hypothermic and ACTH/cortisol responses to the azapirone ipsapirone are attenuated in patients with unipolar depression and panic disorder but not in patients with obsessive-compulsive disorder. The impaired thermic and neuroendocrine responses are associated with increased basal cortisol secretion in depressed patients but not in patients with panic disorder. 3. Chronic treatment with the selective 5-HT reuptake inhibitor fluoxetine decreases 5-HT1A receptor-mediated responses in patients with obsessive-compulsive disorder, while long-term treatment with the tricyclic antidepressant amitriptyline further decreases hypothermia following ipsapirone but has no effect on ACTH/cortisol release. 4. Alteration of the 5-HT1A receptor and/or its signal transduction pathways may play a role in the pathophysiology and treatment of anxiety disorders and depression.
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The rationale for pharmacological treatment of bulimia nervosa is summarized and a review of controlled therapeutic trials shows contradictory results. A number of antidepressant agents (tricyclics: imipramine, desipramine, amitriptyline; IMAO: phenelzine, isocarboxazide; trazodone; fluoxetine) appear more effective than placebo in double-blind controlled trials of 6 to 16 weeks. In similar studies, other antidepressants (mianserine, fluvoxamine) are ineffective. Improvement reported is often incomplete and the low percentage of patients totally abstinent at the end of treatment appears of poor pronostic value for long-term outcome. Methodological limitations of existing studies are discussed, and some psychopathological factors to consider in the assessment of therapeutic response are proposed.
Ten adult insulin-dependent diabetics with symptomatic peripheral neuropathy were treated with amitriptyline alone or in combination with fluphenazine hydrochloride. Nine of the subjects had a good result within 48 to 72 hours. Two patients reacted adversely to the medication. These medications appear effective in treating the discomfort associated with diabetic peripheral neuropathy.
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Systemic treatments for hepatocellular carcinoma (HCC) have been largely unsuccessful. This study investigated the antitumoral activity of Amitriptyline, a tricyclic antidepressant, in hepatoma cells. Amitriptyline-induced toxicity involved early mitophagy activation that subsequently switched to apoptosis. Amitriptyline induced mitochondria dysfunction and oxidative stress in HepG2 cells. Amitriptyline specifically inhibited mitochondrial complex III activity that is associated with decreased mitochondrial membrane potential (∆Ψm) and increased reactive oxygen species (ROS) production. Transmission electron microscopy (TEM) studies revealed structurally abnormal mitochondria that were engulfed by double-membrane structures resembling autophagosomes. Consistent with mitophagy activation, fluorescence microscopy analysis showed mitochondrial Parkin recruitment and colocalization of mitochondria with autophagosome protein markers. Pharmacological or genetic inhibition of autophagy exacerbated the deleterious effects of Amitriptyline on hepatoma cells and led to increased apoptosis. These results suggest that mitophagy acts as an initial adaptive mechanism of cell survival. However persistent mitochondrial damage induced extensive and lethal mitophagy, autophagy stress and autophagolysome permeabilization leading eventually to cell death by apoptosis. Amitriptyline also induced cell death in hepatoma cells lines with mutated p53 and non-sense p53 mutation. Our results support the hypothesis that Amitriptyline-induced mitochondrial dysfunction can be a useful therapeutic strategy for HCC treatment, especially in tumors showing p53 mutations and/or resistant to genotoxic treatments.
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Long term preventive lithium administration results are referred to with the manifestation of a full effect in 23% affective illness-related patients. In 70% of patients, the occurrence of side-effects including those initial ones was stated in no but 40% patients in the course of long term lithium-prophylaxis. This fact testifies about the decrease in number of side-effects during the treatment with lithium. Most frequent side-effects were tremors and diarrhea. No serious renal complications were observed, except the onsets of tardive dyskinesis in on patient after the combined administration of chlorprothixene, amitriptyline and lithium. In three patients, the distant relapses were observed without discontinuation of therapy after the 10-year-lasted successful lithium-prophylaxis. In accord to the long term experience, the authors estimate 0.4 mmol/l lithemia level to be the minimal effective one. They believe the lithium is a reliable thymoprophylactic agent, though in accord with them the other substances with larger therapeutic spectrum are to be searched as well as predictors of an effective lithium-prophylaxis.