Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Withdrawal syndrome after discontinuing serotonin re-uptake inhibitors, especially paroxetine, is largely unknown to most physicians. Variable incidence has been reported. Our aim was to stress the main clinical features of this syndrome. Serotonin re-uptake inhibitor withdrawal syndrome generally begins within 24 to 48 hours after discontinuing the drug. Signs reach their maximum on day 5 and usually resolve within 2 to 3 weeks. Withdrawal syndrome is more common with short half-life drugs (paroxetine, fluvoxamine). The intensity of the clinical signs depends on the daily dose and how long the drug has been given. The main signs are dizziness, vertigo, headache, nausea, and flu-like symptoms as well as anxiety, confusion, irritability, excessive dreaming and insomnia. Risk factors usually stressed are poor treatment compliance, previous withdrawal syndrome with another drug, concomitant medication and alcohol consumption. The syndrome can be prevented by tapering off the dose and patient education. When a withdrawal syndrome is present, it is advisable to reintroduce the drug then withdraw gradually.
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PMID:[Paroxetine withdrawal syndrome]. 1085 79

Amantadine, an inhibitor of M2 ion channel of influenza A virus, is an oral antiviral drug which specifically inhibits the uncoating and viral replication of the influenza A virus. Studies have shown that amantadine treatment within 48 hours of acute infection of influenza A reduces fever within 24 hours and shortens the course of illness. Amantadine has been found to have an efficacy of 50 to 90% prevention of illness. However amantadine-resistant viruses have been recovered approximately 30% patients treated with amantadine, as early as 2-3 days into treatment. Side effects of insomnia, decreased concentration and dizziness have been reported in 5 to 33% of amantadine recipients. Therefore amantadine should be only used for influenza A infected high risk persons.
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PMID:[Anti-influenza A viral drug--amantadine]. 1122 19

This multicenter, randomized, controlled study evaluated the efficacy and safety of interferon alfacon-1 (r-IFN-alphacon1) compared with lymphoblastoid interferon-alpha (IFN-alphan1) in patients with high-titer chronic hepatitis C virus (HCV) infection. Two hundred and seven patients were randomized to receive either 18 MIU (&mgr;g) r-IFN-alphacon1 or 9 MIU IFN-alphan1 daily for 2 weeks, followed by the administration of the study drugs three times weekly for 22 weeks. The primary endpoint was sustained virological response defined as the inability to detect serum HCV RNA at the end of the 24 week post-treatment observation period. In the intention-to-treat analysis, r-IFN-alphacon1 produced a slightly but not significantly higher proportion of sustained virological response than IFN-alphan1 (26.3 vs. 20.7% P=0.392). In patients with high baseline titer and genotype 1b, the proportion of sustained virological response was significantly higher in the r-IFN-alphacon1 cohort, than the IFN-alphan1 cohort (16.7 vs. 3.3%, P=0.017). The adverse events commonly reported were flu-like symptoms, anorexia, insomnia, and alopecia. Types and frequencies of the adverse events were similar in the two cohorts. The results of this study show that r-IFN-alphacon1 is an effective and tolerable therapy in patients with chronic HCV with high viral titer. The results also indicate that 18 MIU r-IFN-alphacon1 is superior in efficacy without additional toxicity to 9 MIU IFN-alphan1 in high-titer chronic HCV patients, particularly with genotype 1b.
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PMID:A multicenter, randomized, controlled clinical trial of interferon alfacon-1 in comparison with lymphoblastoid interferon-alpha in patients with high-titer chronic hepatitis C virus infection. 1180 28

In 1916, von Economo first described encephalitis lethargica (EL), a CNS disorder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkinsonism) and neuropsychiatric sequelae. Since the 1916-1927 epidemic, only sporadic cases have been described. Pathological studies revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell) infiltration. The EL epidemic occurred during the same time period as the 1918 influenza pandemic, and the two outbreaks have been linked in the medical literature. However, von Economo and other contemporary scientists thought that the 1918 influenza virus was not the cause of EL. Recent examination of archived EL brain material has failed to demonstrate influenza RNA, adding to the evidence that EL was not an invasive influenza encephalitis. By contrast, the findings of intrathecal oligoclonal bands (OCB) and beneficial effects of steroid treatments have provoked the hypothesis that EL may be immune-mediated. We have recently seen 20 patients with a similar EL phenotype, 55% of whom had a preceding pharyngitis. The patients had remarkable similarity to the historical descriptions of EL: sleep disorder (somnolence, sleep inversion or insomnia), lethargy, parkinsonism, dyskinesias and neuropsychiatric symptoms. CSF examination commonly showed elevated protein and OCB (75 and 69% respectively). Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism. MRI of the brain was normal in 60% but showed inflammatory changes localized to the deep grey matter in 40% of patients. We investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea. Anti-streptolysin-O titres were elevated in 65% of patients. Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens. These antibodies were also present in the CSF in four patients tested. By contrast, antibodies reactive against the basal ganglia were found in only 2-4% of child and adult controls (n = 173, P < 0.0001). Rather than showing polyspecific binding, these antibodies bound to common neural autoantigens of molecular weight 40, 45, 60 and 98 kDa. Regional tissue comparisons showed that the majority of these autoantigens were specific to or enriched in CNS tissue. Immunohistochemistry with secondary staining localized antibody binding to neurons rather than glial populations. Further investigation is required to determine whether these antibodies affect neuronal function (i.e. whether they are pathogenic anti-neuronal antibodies). Histopathology in one case demonstrated striatal encephalitis with perivenous B- and T-lymphocytic infiltration. We believe an EL-like syndrome is still prevalent, and propose that this syndrome may be secondary to autoimmunity against deep grey matter neurons.
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PMID:Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity. 1467 31

Interferon-alpha (IFN) is widely used for the treatment of viral illnesses and other chronic diseases, though its usefulness is hampered by a problematic side-effect profile. In particular, IFN-alpha induces neuropsychiatric and neurotoxic side effects, including depression, anxiety, insomnia, lethargy, confusion, and psychosis. Of particular interest, a number of patients develop full psychiatric syndromes, particularly depressive disorders. Recent evidence suggests that conventional antidepressants (especially selective serotonin reuptake inhibitors) are effective in preventing or reducing IFN-induced side-effects, but even these compounds are not 100% effective in preventing these symptoms. As such, alternative treatments must be considered. Non-steroidal anti-inflammatory drugs (NSAIDs) are known to counteract a number of IFN-induced side effects, including cytokine activation, stress hormone release, and neurochemical alterations (reduced 5-HT [serotonin]). NSAIDs are widely recommended for various aspects of flu-like symptoms or sickness behaviors in humans, including those induced specifically by IFN. In addition, NSAIDs appear to be effective in treating premenstrual dysphoric disorder. These data indirectly specify a role for NSAIDs in syndromes with a prominent depression component. Drawing from an extensive pre-clinical and clinical research base, we hypothesize that pretreatment with NSAIDs will not only reduce the incidence of flu-like symptoms, but also prove effective for the prevention or reduction of IFN-induced depression.
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PMID:IFN-induced depression: a role for NSAIDs. 1460 39

To evaluate long-term efficacy and tolerability of the serotonin 5-HT1A receptor agonist, gepirone extended release (ER), a multicenter, randomized, placebo-controlled relapse prevention study was performed in patients with recurrent major depression (DSM-IV criteria). Patients 18 to 70 years, with a primary diagnosis of recurrent major depression (DSM-IV; 296.3) and a screening and baseline HAMD-17 total score >/=20 were eligible. After a 3- to 14-day (dependent on pretrial medication) single-blind placebo washout period, eligible patients entered an 8- or 12-week (depending on time to remission) open-label gepirone ER treatment period. They initially received a dose of 20 mg/d gepirone ER and were titrated to a dose of 40 to 80 mg/d. Patients who achieved remission (HAMD-17 total score </=8) were randomized to double-blind continuation of their gepirone ER treatment or placebo for 40 to 44 weeks. The primary end point was a comparison of the relapse rates between gepirone ER and placebo. Relapse was defined as a HAMD-17 total score >/=16 or discontinuation for lack of efficacy. A total of 420 patients were treated in the open-label phase. Of these, 303 (72.1%) completed the open-label phase and 250 (59.5%) fulfilled the criteria for remission and were randomized into the double-blind continuation phase (gepirone ER: n = 126; placebo: n = 124). The mean (+/-SD) final titrated dose of gepirone ER was 61.9 (+/-17.0) mg/d in the double-blind continuation phase. The relapse rate in the gepirone ER group was statistically significantly lower than that in the placebo group, 23.0% versus 34.7%, respectively (P = 0.024). During the open-label phase, adverse events that occurred in more than 5% of patients were nausea (15.7%), dizziness (13.1%), headache (12.9%), insomnia (6.2%), and vertigo (6.0%). During the continuation phase, the incidence of newly or re-emerging adverse events was similar with gepirone ER (43.7%) and placebo (42.7%). Adverse events different from those occurring during the open-label phase were not apparent. All adverse events occurred in less than 5% of patients with the exception of flu syndrome and headache. In conclusion, gepirone ER at a dose range of 40 to 80 mg/d is effective for relapse prevention in patients with recurrent major depression. It is well tolerated during long-term treatment for up to approximately one year.
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PMID:Relapse prevention with gepirone ER in outpatients with major depression. 1564 3

Anorexia is a common symptom accompanying infections, but the teleology of the phenomenon remains unexplained. We hypothesize that anorexia may represent a prehistoric behavioral adaptation to fight infection by maintaining T helper (Th)2 bias, which is particularly vital in fighting bacterial pathogens. Specifically, we propose that anorexia may avert the reduction of Th2/Th1 ratio by preventing feeding-induced neurohormonal and vagal output from the gut. Emerging evidence suggests that the vagal and neurohormonal output of the gut during feeding promotes Th1 function, which is desirable in fighting viral infections. Since fever may be an adaptation to fight bacteria and "colds" are generally viral in origin, the adage "starve a fever and feed a cold" may reflect a sensible behavioral strategy to tilt autonomic and Th balance in directions that are optimal for fighting the particular type of infection. The ability to modulate T helper balance through the neurohormonal and autonomic axis by adjusting food intake may be the mechanism behind other unexplained clinical observations such as the improved outcomes of ICU patients after enteric versus parenteric feedings. Compared to the prehistoric period when bacterial infection was commonplace, the anorexic response may be less adaptive today when viruses and cancers have become common triggers of anorexia. By promoting host anorexia, cachexia, and insomnia, cancers and viruses can deter behaviors such as digestion and sleep that would raise vagal and Th1 activity against tumors and viruses. Hydration and sleep, unexplained but widely accepted recommendations for flu patients, may also work by promoting vagal and Th1 functions. Modulating feeding, hydration, and sleep may prove beneficial in treating other conditions associated with abnormal autonomic and Th balance.
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PMID:"Starve a fever and feed a cold": feeding and anorexia may be adaptive behavioral modulators of autonomic and T helper balance. 1582 88

Antidepressant discontinuation syndrome occurs in approximately 20 percent of patients after abrupt discontinuation of an antidepressant medication that was taken for at least six weeks. Typical symptoms of antidepressant discontinuation syndrome include flu-like symptoms, insomnia, nausea, imbalance, sensory disturbances, and hyperarousal. These symptoms usually are mild, last one to two weeks, and are rapidly extinguished with reinstitution of antidepressant medication. Antidepressant discontinuation syndrome is more likely with a longer duration of treatment and a shorter half-life of the treatment drug. A high index of suspicion should be maintained for the emergence of discontinuation symptoms, which should prompt close questioning regarding accidental or purposeful self-discontinuation of medication. Before antidepressants are prescribed, patient education should include warnings about the potential problems associated with abrupt discontinuation. Education about this common and likely underrecognized clinical phenomenon will help prevent future episodes and minimize the risk of misdiagnosis.
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PMID:Antidepressant discontinuation syndrome. 1691 64

Theratechnologies, under license from Valeant, is developing tesamorelin as a potential vaccine adjuvant and for the potential treatment of wasting, hip fracture recovery, immune disorders, HIV-related lipodystrophy, sleep maintenance insomnia and mild cognitive impairment. Phase III clinical trials for the treatment of HIV-associated lipodystrophy and phase II clinical trials for sleep disorder, chronic obstructive pulmonary disorder, hip fracture and immune system dysfunction are underway. Phase II trials are also assessing the influenza vaccination immune response and cognitive effects of tesamorelin.
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PMID:Drug evaluation: tesamorelin, a synthetic human growth hormone releasing factor. 1708 39

Early and maintained treatment is important for better long-term outcomes in schizophrenia. We hypothesized that treatment with injectable risperidone long-acting therapy (RLAT) would be associated with improved outcomes in recently diagnosed patients compared with those having longer illness duration. Post-hoc analyses were conducted from a 1-year study of stable patients receiving RLAT (25 or 50 mg every 2 weeks) to compare patients diagnosed with schizophrenia in < or ears (recently diagnosed; n=57) with those diagnosed more than 3 years (n=266). Relapse rates were 10.5 and 21.8%, respectively [P=0.053, chi(2)azard ratio 2.2 (95% confidence interval=0.95, 5.13)]. Both groups improved significantly in mean total Positive and Negative Syndrome Scale and Clinical Global Impressions-Severity (CGI-S) scores (P<0.01). Recently diagnosed patients showed greater improvement versus patients diagnosed for more than 3 years in adjusted mean Positive and Negative Syndrome Scale total (-10.2+/-2.0 vs. -3.8+/-0.9; P=0.004) and Clinical Global Impressions-Severity (-0.5+/-0.1 vs. -0.2+/-0.1; P=0.002) scores. The most common adverse events were insomnia (31.6 vs. 26.7%), psychiatric disorders (19.3 vs. 20.7%), headache (15.8 vs. 19.2%), anxiety (12.3 vs. 17.3%), and influenza (10.5 vs. 5.3%). These findings confirm the benefit of RLAT in patients with schizophrenia and suggest that earlier treatment with long-acting preparations is associated with better outcomes.
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PMID:Risperidone long-acting therapy in stable patients with recently diagnosed schizophrenia. 2010 Nov 85


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