Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fragile X syndrome is the leading inherited form of mental retardation, and second only to Down's syndrome as a cause of mental retardation attributable to an identifiable genetic abnormality. Fragile X syndrome is caused by a defect in the fragile X mental retardation 1 gene (FMR1), located near the end of the long arm of the X chromosome. FMR1 normally synthesises the fragile X protein (FMRP), but mutations in FMR1 lead to a lack of FMRP synthesis, resulting in fragile X syndrome. While the specific function of FMRP is not yet fully understood, the protein is known to be important for normal brain development. The physical, cognitive and behavioural features of individuals with fragile X syndrome depend on gender (females have two X chromosomes, one active and one inactive) and the molecular status of the mutation (premutation, full mutation or mosaic). Features of the behavioural profile of individuals with fragile X syndrome include hypersensitivity to stimuli, overarousability, inattention, hyperactivity and (mostly in men) explosive and aggressive behaviour to others or self. Social anxiety, other anxiety disorders, depression, impulse control disorder and mood disorders are the most common psychiatric disorders diagnosed in individuals with fragile X syndrome, although no formal studies have been undertaken. There have been very few psychopharmacological studies of the treatment of behaviours associated with fragile X syndrome. These limited studies and surveys of psychotropic drugs used in individuals with fragile X syndrome suggest that stimulants are helpful for hyperactivity, that alpha(2)-adrenoceptor agonists and beta-adrenoceptor antagonists help to control overarousability, impulsivity and aggressiveness, and that SSRIs can control anxiety, impulsivity and irritability, alleviate depressive symptoms and decrease aggressive and self-injurious behaviour. Typical and atypical antipsychotics in combination with other psychotropics have been used for control of psychotic disorders and severe aggressive behaviours. Mood stabilisers have been found to be useful when mood dysregulation or mood disorders are present with or without aggressive behaviour. Folic acid and L-acetylcarnitine (levacecarnine) have not been found to improve deficits or behaviours. As there is no specific psychotropic drug for any of the deficits or behaviours associated with fragile X syndrome, clinicians are advised to diagnose any psychiatric syndromes or disorders present and treat them with the appropriate psychotropic drug. If no psychiatric disorder can be diagnosed and the patient's challenging behaviours cannot be controlled with environmental manipulation or behaviour modification techniques, the most benign psychotropic drug should be used. Antipsychotics should be reserved for psychotic disorders, for impulse control disorders (used in combination with other psychotropics), or when challenging behaviours constitute an emergency. In the future, new medications targeting molecules implicated in the modulation of anxiety, fear and fear responding will be useful for treating the social anxiety and overarousability exhibited by individuals with fragile X syndrome.
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PMID:Neuropsychiatric symptoms of fragile X syndrome: pathophysiology and pharmacotherapy. 1533 Jun 85

The management of adverse premenstrual symptoms has presented a difficult challenge for clinicians. However, based on numerous well-designed research studies over the last decade, we now have diagnostic criteria for the severe form of the syndrome, premenstrual dysphoric disorder, and a variety of evidence-based therapeutic strategies. This review presents a comprehensive, practical description of what the clinician needs to know to diagnose and treat adverse premenstrual symptoms at all levels of severity. Diagnostic criteria are described in detail, including a discussion of the distinction between premenstrual dysphoric disorder and premenstrual syndrome (PMS). The rationale for including prospective symptom calendars as a routine part of the diagnostic evaluation of severe symptoms is presented. The differential diagnosis of cyclic symptoms, including depression and anxiety disorders, menstrual migraine, and mastalgia, and an approach for the management of each of these problems are presented. A treatment approach is recommended that matches the treatment to the degree of problems the woman is experiencing. Serotonin reuptake inhibitors are the treatment of choice for severe symptoms, and most women with PMS/premenstrual dysphoric disorder will respond to intermittent, luteal phase-only therapy. Ovulation suppression should be reserved for women who do not respond to other forms of therapy. The role of oophorectomy is limited, and guidelines for its use are presented.
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PMID:Premenstrual syndrome, premenstrual dysphoric disorder, and beyond: a clinical primer for practitioners. 1545 9

The striatum has been consistently implicated in the pathophysiology of obsessive-compulsive disorder (OCD), yet, studies assessing the performance of OCD patients in procedural learning tasks, assumed to rely on the intact functioning of the striatum, have yielded inconsistent results. Recently, Rauch et al. [Rauch SL, Savage CR, Alpert NM, Dougherty D, Kendrick A, Curran T, et al. Probing striatal function in obsessive-compulsive disorder: a PET study of implicit sequence learning. J Neuropsychiatry Clin Neurosci 1997;9:568-73] have obtained evidence suggesting that seemingly intact performance of OCD patients in such tasks may be achieved by recruiting systems which in normal subjects are reserved for explicit or declarative, rather than implicit or procedural, processing. The present study assessed procedural learning in OCD patients using a card betting task in which explicit processing impairs, rather than assists, acquisition. In addition, we tested a group of Parkinson's disease (PD) patients, in order to better establish the dependence of the task on procedural learning, and a group of major depressive disorder (MDD) patients, in order to test the possibility that impaired learning in the card betting task may be a result of concurrent depression. The majority of OCD (15/18) and PD patients (14/16) did not acquire the task, whereas MDD patients acquired the task similarly to normal control subjects. These results demonstrate that OCD patients are impaired on a procedural learning task in which explicit processing impairs acquisition. Two different interpretations are suggested: that the striatal system is dysfunctional in OCD, or that inappropriate explicit processing in OCD interferes with the functioning of the striatal system.
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PMID:Impaired procedural learning in obsessive-compulsive disorder and Parkinson's disease, but not in major depressive disorder. 1563 76

Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.
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PMID:Neuropsychiatric adverse effects of interferon-alpha: recognition and management. 1569 25

When psychological and behavioral disorders of Alzheimer's disease appear suddenly, somatic, iatrogenic and reactive or relational psychological causes must be ruled out or treated before concluding that the cause is lesional. Non-pharmacological interventions should be privileged for the prevention and management of behavioral manifestations of mild to moderate intensity: psychological support of the patient (short therapies), training the caregiver, work on daily habits, reorganization of the home, behavioral measures against apathy and especially agitation, rehabilitation strategies, and therapy involving music, light, aromas, etc. Pharmacological therapies are only moderately effective in these disorders. They must be targeted and follow a sequence of prescription that maximizes tolerance and distinguishes treatment of acute and chronic states. Anticholinesterase agents may be useful in this domain to prevent or ease some symptoms (especially apathy). The efficacy of memantine must be confirmed by additional data. Some selective serotonin reuptake inhibitors agents may be useful not only in depression but also anxiety, emotional disturbances, irritability and compulsiveness. Atypical neuroleptics are better tolerated than the classic ones. They are most effective in this context but must be reserved for specific indications and limited in time because of the increased risk of stroke. Other psychotropics (benzodiazepines, carbamates, antiepileptics) should be used cautiously in this context.
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PMID:[Treatment of the psychological and behavioural disorders of Alzheimer's disease]. 1598 46

In 181 urban African Americans with Type 2 diabetes, medication adherence was assessed using a measure designed specifically for an urban, impoverished sociodemographic population. Hemoglobin A-sub(1c), blood pressure and cholesterol levels, medication-related beliefs, and depression were assessed. Seventy-four percent of the sample reported adherence to diabetes medication. Adherence, adjusted for age, was associated with lower hemoglobin A-sub(1c). The specific behaviors associated with poorer diabetes control were forgetting to take medications and running out of medications. Knowledge of blood glucose goals differed for adherers and nonadherers. Blood pressure and cholesterol medication adherence rates were not associated with actual levels of blood pressure or lipids, respectively. These data suggest that specific medication-taking behaviors are important to diabetes control and constitute logical targets for interventions. ((c) 2005 APA, all rights reserved).
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PMID:Medication adherence and diabetes control in urban African Americans with type 2 diabetes. 1604 70

To investigate the interactive process of changes in social anxiety and depression during treatment, the authors assessed weekly symptoms in 66 adult outpatients with social phobia (social anxiety disorder) who participated in cognitive- behavioral group therapy. Multilevel mediational analyses revealed that improvements in social anxiety mediated 91% of the improvements in depression over time. Conversely, decreases in depression only accounted for 6% of the decreases in social anxiety over time. Changes in social anxiety fully mediated changes in depression during the course of treatment. The theoretical and clinical implications of these findings for the relationship between anxiety and depression are discussed. reserved).
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PMID:Mediation of changes in anxiety and depression during treatment of social phobia. 1628 94

The stress is defined as a self perceived negative or unpleasant impact. Distress is reserved for the experience of specific symptoms such as anxiety or depression. The term stressor covers some environmental circumstances directly or indirectly affecting the individual. As Selye has suggested, we must remember that stress is the great equalizer of biological activities. If we use the same parts of our bodies or minds over and over again, nature has only stress with which to face us out of the routine. As a consequence, unhealthy levels of stress lead to a variety of disorders and illness.
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PMID:[Effects of psychological stress on health]. 1661 Jan 63

Background In patients with non-ST elevation acute coronary syndrome (NST-ACS) that is treated invasively, glycoprotein (GP) IIb/IIIa inhibitors can be used either as upstream treatment in a coronary care unit or as downstream provisional treatment in selected patients who are undergoing percutaneous coronary intervention (PCI). The relative advantage of either strategy is unknown. The purpose of this study was to assess 30-day outcome of patients enrolled in a prospective NST-ACS registry and treated invasively with either of these two therapeutic strategies. Methods Patients treated invasively (coronary arteriography within 4 days of admission), in the prospective registry ROSAI-2, were divided into two groups according to the upstream use of GPIIb/IIIa inhibitors (n = 241), or not (n = 548). In the latter group, 76 (14%) patients received GPIIb/IIIa in association with a PCI procedure. Clinical and angiographic characteristics as well as in-hospital and 30-day outcome of these two groups of patients were compared. Results The two groups were similar with respect to age, sex, presence of hypertension, diabetes, number of PCI procedures. However, patients treated with upstream GPllb/llla blockers had more frequently ST-segment depression (P = 0.002), a high TIMI risk score (P = 0.01) and were more frequently admitted to centres with Cath Lab facilities (P = 0.001). At 30-day follow-up, the composite of death, acute myocardial infarction and stroke, as well as major bleeding, was not significantly different between the two groups, although it occurred more frequently in patients who received upstream GPIIb/IIIa blockers (9.5% versus 5.7% and 1.7% versus 0.2%, respectively). By multivariate analysis, diabetes [odds ratio (OR) = 2.22, 95% confidence interval (CI) = 1.2-4.09] and a diagnosis on admission of non-Q-wave myocardial infarction (OR = 2.0, 95% Cl = 1.10-3.6) were independently related to outcome. No additional risk or benefit was related to upstream GPIIb/IIIa inhibitor treatment (OR = 1.5, 95% Cl = 0.84-2.68). Conclusions Among invasively-treated patients with NST-ACS, upstream treatment with GPIIb/IIIa inhibitors was used in those with a higher clinical risk profile, whereas downstream treatment was reserved for a limited number of patients undergoing PCI. Thirty-day outcome was similar in the two groups, irrespective of the treatment strategy used.
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PMID:Use of glycoprotein IIb/IIIa inhibitors in invasively-treated patients with non-ST elevation acute coronary syndrome. 1664 80

In 2003, there were 28,092 human exposures to diphenhydramine reported to poison centers in the US. A related drug, dimenhydrinate, is a less frequent cause of poisonings. Between January 2000 and June 2004, there were 2,534 reported dimenhydrinate ingestions in children less than 6 years of age. An evidence-based expert consensus process was used to create this guideline. Relevant articles were abstracted by a trained physician researcher. The first draft was created by the primary author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with a suspected ingestion of diphenhydramine or dimenhydrinate, or a dermal exposure to diphenhydramine. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. The panel's recommendations for dermal or oral exposures to diphenhydramine or oral exposures to dimenhydrinate follow. The grade of recommendation is in parentheses: 1) All patients with suicidal intent, intentional abuse, or in cases in which a malicious intent is suspected (e.g., child abuse or neglect) should be referred to an emergency department (Grade D). 2) In patients without evidence of self-harm, abuse, or malicious intent, poison center personnel should elicit additional information including the time of the ingestion or dermal exposure, determination of the precise dose ingested, and the presence of co-ingestants (Grade D). 3) Patients experiencing any changes in behavior other than mild drowsiness or mild stimulation should be referred to an emergency department. Examples of moderate to severe symptoms that warrant referral include agitation, staring spells, inconsolable crying, hallucinations, abnormal muscle movements, loss of consciousness, seizures, or respiratory depression (Grade D). 4) For patients referred to the emergency department, transportation via ambulance should be considered based on several factors including the condition of the patient and the length of time it will take the patient to arrive at the emergency department (Grade D). 5) If the patient has no symptoms, and more than 4 hours have elapsed between the time of diphenhydramine ingestion and the call to the poison center, referral to an emergency department is not recommended. For dermal exposures to diphenhydramine, if the patient has no symptoms and it has been more than 8 hours since the diphenhydramine was thoroughly removed from the skin, referral to an emergency department is not recommended (Grade D). 6) Patients with acute ingestions of less than a toxic dose of diphenhydramine, or chronic exposures to diphenhydramine and no or mild symptoms, can be observed at home with instructions to call the poison center back if symptoms develop or worsen. The poison center should consider making a follow-up call at approximately 4 hours after ingestion (Grade D). 7) Children less than 6 years of age who ingest at least 7.5 mg/kg of diphenhydramine should be referred to an emergency department (Grade D). 8) Patients 6 years of age and older who ingest at least 7.5 mg/kg or 300 mg of diphenhydramine (whichever is less), should be referred to an emergency department (Grade D). 9) If the patient has no symptoms, and more than 6 hours have elapsed between the time of dimenhydrinate ingestion and the call to the poison center, referral to an emergency department is not recommended (Grade D). 10) Patients with acute ingestions of less than a toxic dose of dimenhydrinate, or chronic exposures to dimenhydrinate and no or mild symptoms, can be observed at home with instructions to call the poison center back if symptoms develop or worsen. The poison center should consider making a follow-up call at approximately 6 hours after ingestion (Grade D). 11) Children less than 6 years of age ingesting at least 7.5 mg/kg of dimenhydrinate should be referred to an emergency department (Grade D). 12) Patients 6 years of age and older ingesting at least 7.5 mg/kg or 300 mg of dimenhydrinate (whichever is less), should be referred to an emergency department for evaluation (Grade D). 13) Following oral exposures of diphenhydramine or dimenhydrinate, do not induce emesis. Because of the potential for diphenhydramine or dimenhydrinate to cause loss of consciousness or seizures, activated charcoal should not be administered en route to an emergency department (Grade D). 14) For chronic dermal exposures of diphenhydramine, skin decontamination (with water or soap and water) should be attempted prior to transporting a patient to an emergency department unless moderate to severe symptoms are already present. In this circumstance, transportation should not be delayed, and EMS personnel should attempt skin decontamination en route to the emergency department (Grade D). 15) Intravenous sodium bicarbonate may be administered by EMS personnel if QRS widening (QRS >0.10 msec) is present and if authorized by EMS medical direction (Grade D). 16) Physostigmine should be reserved for administration in a hospital (Grade D). 17) Benzodiazepines may be administered by EMS personnel if agitation or seizures are present, and if authorized by EMS medical direction (Grade D).
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PMID:Diphenhydramine and dimenhydrinate poisoning: an evidence-based consensus guideline for out-of-hospital management. 1674 37


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