Depression
Quentin Spender, Judith Barnsley, Alison Davies, Jenny Murphy in Primary Child and Adolescent Mental Health, 2019
Clinical practice suggests that antidepressants make depressive disorder better. This may be partly due to a placebo effect, but research suggests that they are almost twice as effective as placebo.20 Clinical guidelines recommend starting a selective serotonin reuptake inhibitor such as fluoxetine as part of the initial treatment for severe depression (preferably in conjunction with some talking treatment) and after a period of psychological treatment in moderate depression.21 There has been much debate about an increase in suicidal thoughts and self-harm in the few weeks after starting medication, an effect that seems to be more likely in adolescents than adults.22 It seems however that the risk of completed suicide is greater if the depression is not treated with everything available, including medication: the benefits of antidepressants appear to be much greater than the risks from suicidal ideas or attempts.23
Topic 11 Consultation Liaison Psychiatry
Melvyn W.B. Zhang, Cyrus S.H. Ho, Roger C.M. Ho, Basant K. Puri in Get Through, 2016
Management: Psychiatrists should advice medical colleagues or general practitioners (GPs) to gradually reduce the frequency of visits and unnecessary investigations by increasing the duration between appointments. Antidepressants such as selective serotonin reuptake inhibitor (SSRI) are useful. Psychotherapy is useful to treat the disorder: Cognitive therapy: reattribution and developing alternative explanations of symptoms and concerns of serious illness. Cognitive restructuring can modify dysfunctional assumptions.Behavioural therapy: self-monitoring of worries, negative thoughts and illness-related behaviours. It also involves exposure and response prevention and reducing repeated reassurance-seeking behaviours.Relaxation techniques.
Management of poisoning
Bev-Lorraine True, Robert H. Dreisbach in Dreisbach’s HANDBOOK of POISONING, 2001
Hyperthermia can be caused by: drug side-effects or interactions: muscular overactivity, disrupted thermoregulation or increased metabolic rate. Side-effects or interactions:anesthetic or phenothiazine side-effect, serotonin syndrome from drug interactions such as monoamine oxidase inhibitor + selective serotonin reuptake inhibitor (SSRI), monoamine oxidase inhibitor + meperidine, or SSRI + St John’s wort, etc.Poisons that cause muscular overactivity (seizures) or rigidity:amoxapine, amphetamine, cocaine, LSD, maprotiline, phencyclidine (PCP), tricyclic antidepressants.Disrupted thermoregulation:any anticholinergic agent, malignant hyperthermia from some general anesthetics (halothane and succinylcholine), or neuroleptic malignant syndrome (phenothiazines).Increased metabolic rate:dinitrophenol, salicylates, thyroid hormone, and pentachlorophenol.
Chronic subjective dizziness among an aging population is associated with amyloid positron emission tomography and neuropsychiatric symptoms
Published in Hearing, Balance and Communication, 2022
Fourth, there is evidence that CSD can be managed by three main forms of treatment that can be used in combination to maximize potential benefits. These forms include Vestibular therapy (a form of physical therapy), Cognitive-behavioral therapy, and Selective serotonin reuptake inhibitors (normally used to treat depression) [31–35]. Interestingly, these forms of interventions have been found to reduce the rate of Aβ deposition in human or animal studies. For example, selective serotonin reuptake inhibitor antidepressants found to reduce Aβ levels in humans [36]. This evidence was also found in animal studies [37]. Given that elevated anxiety symptoms may exacerbate Aβ-related cognitive impairment, cognitive-behavioral therapy is one of the important management options that may reduce the Aβ levels. Whether the management of CSD in ageing adults via these options can reduce Aβ deposition and delay the onset of AD requires large-scale randomized controlled trials with long follow-up periods.
Review of the clinical approach to the treatment of disruptive mood dysregulation disorder
Published in International Review of Psychiatry, 2020
Brian Hendrickson, Mahlet Girma, Leslie Miller
There has been limited pharmacologic research for the treatment of youth with irritable and dysregulated mood. The majority of studies assess youth with ADHD and a disruptive behaviour disorder and/or irritability, with only a few studies enrolling children with both ADHD and DMDD, and one study of children with SMD alone. Furthermore, the majority of studies are small RCTs or open-label studies. Based on the literature and clinical experience, it is reasonable to proceed with stimulant optimization first for children diagnosed with ADHD and DMDD. Further research is required to determine whether stimulants would be beneficial in children with DMDD without ADHD. For treatment refractory irritability or aggression, augmentation with a second generation neuroleptic, particularly risperidone or aripiprazole, or a mood stabilizer such as valproic acid may be considered. Due to concern for side effects of these augmentation agents however, a careful assessment of mood and anxiety symptoms that may be targeted with an evidence based serotonin selective reuptake inhibitor (SSRI) may be beneficial. This may be especially relevant for youth who meet criteria for DMDD but do not meet criteria for ADHD. Data do not support the use of lithium for youth with DMDD.
Inhibitory Control in Male and Female Adolescents with Autism Spectrum Disorder (ASD)
Published in Developmental Neuropsychology, 2022
Mackenzie N. Cissne, Katherine R. Bellesheim, Shawn E. Christ
Individuals with color blindness, severe cognitive impairment, or major medical history unrelated to ASD were excluded from the study. Eight ASD participants were prescribed attention-related medications or other medications known to affect cognitive performance (e.g., methylphenidate, amphetamine, Concerta). They were able to safely refrain (per their treating physicians) from taking the relevant medication for 24 hours prior to testing and thus were included in the study. Other medications included serotonin-norepinephrine reuptake inhibitor (SNRI; ASD = 7), guanfacine (ASD = 2), propranolol (ASD = 1), selective serotonin reuptake inhibitors (SSRI; ASD = 4, non-ASD = 2), buspirone (ASD = 2), tetracyclic antidepressant (ASD = 1), and/or antipsychotics (second generation or atypical; ASD = 3). Because of safety reasons and/or their relatively long half-lives, these medications were not withheld for the purposes of the present study.
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