Альтернативные методы коррекции СДВГ

Bacopa monnieri is an Ayurvedic medicinal herbal widely used as a tonic and memory enhancer. In a small 12-week double-blind RCT, 36 children with ADHD randomized to receive Bacopa, 50 mg BID, showed significant improvement over placebo in tests of sentence repetition, logical memory, and pair-associative learning.

A standardized extract of the bark from the French maritime pine (Pinus pinaster) may also help reduce symptoms of ADHD. A total of 61 children and adolescents randomized to a standardized extract of French maritime pine bark (Pycnogenol™), 1 mg/kg/d, for 1 month, experienced significant improvements in hyperactivity, inattention, and visual-motor coordination compared with placebo recipients; symptoms returned to pre-treatment baseline levels after a 1-month washout.

There is also promising evidence that zinc supplementation may mitigate ADHD symptoms. In a large 12-week double-blind placebo controlled trial (N = 400), children and adolescents randomized to a high dose of zinc, 150 mg/d, experienced significant improvement in hyperactivity and impulsivity but not inattention over placebo. In an augmentation study, the addition of zinc to methylphenidate resulted in greater improvement than methylphenidate alone.

 Alternative Medicine Therapies for ADHD

Психостимуляторы для пожилых больных

Psychostimulants are recognized for their role in managing attention-deficit/hyperactivity disorder
(ADHD), but also have found a treatment niche in conditions such as apathy, fatigue, and depression.

Psychostimulants for older adult

Сравнительный анализ атомоксетина и метилфенидата при СДВГ

Background
Psychostimulants and non stimulants are effective in the treatment of ADHD. Efficacy of both methylphenidate and atomoxetine has been established in placebo controlled trials. Direct comparison of efficacy is now possible due to availability of results from several head-to-head trials of these two medications.
Methods
All published, randomized, open label or double blind trials, comparing efficacy of methylphenidate with atomoxetine, in treatment of ADHD in children, diagnosed using DSM-IVTM criteria were included. The outcome studied was ADHDRS-IVParent:Inv score. The standardized mean difference (SMD) was used as a measure of effect size.
Results
Nine randomized trials comparing methylphenidate and atomoxetine, with a total of 2762 participants were included. Meta-analysis did not find a significant difference in efficacy between methylphenidate and atomoxetine (SMD= 0.09, 95% CI -0.08-0.26) (Z=1.06, p=0.29). Synthesis of data from eight trials found no significant difference in response rates (RR=0.93 95% CI 0.76-1.14, p=0.49). Sub group analysis showed a significant standardized mean difference favouring OROS methylphenidate (SMD=0.32, 95% CI 0.12-0.53 (Z=3.05, p<0.002). Immediate release methylphenidate was not superior to atomoxetine (SMD= -0.04, 95% CI -0.19-0.12) (Z=0.46, p=0.64). Excluding open label trials did not significantly alter the effect size (SMD=0.08, 95% CI -0.04-0.21) (Z=1.27, p=0.20). All-cause discontinuation was used as a measure of acceptability. There was no significant difference in all cause discontinuation between atomoxetine and methylphenidate (RR 1.22, 95% CI 0.87-1.71). There was significant heterogeneity among the studies (p=0.002, I2=67%). Subgroup analysis demonstrated the heterogeneity to be due to the open label trials (p=0.001, I2=81%).
Conclusions
In general atomoxetine and methylphenidate have comparable efficacy and equal acceptability in treatment of ADHD in children and adolescents. However OROS methylphenidate is more effective than atomoxetine and may be considered as first line treatment in treatment of ADHD in children and adolescents.

Comparative efficacy and acceptability of methylphenidate and atomoxetine in treatment of attention deficit hyperactivity disorder in children and adolescents: a meta-analysis

Фармакотерапия когнитивных нарушений при травмах головного мозга

Recommended treatments for mild TBI-related cognitive deficits

Deficit	First-line medication	Side effects	Contraindications	Other treatments
Memory	Donepezil (5 to 10 mg/d)	Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia	Hypersensitivity to donepezil or piperidine derivatives	Rivastigmine, galantamine, physostigmine, CDP-choline
Speed of processing	Methylphenidate (0.3 mg/kg twice daily)	Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability	Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days	Dextroamphetamine
Executive function	Amantadine (200 to 400 mg/d)	CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia	Hypersensitivity to amantadine	Bromocriptine, pramipexole, carbidopa/levodopa
CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor
Source:Reference 8

Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.

Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10

Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11

Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8

Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.

Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.

Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23

The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26

Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.

Traumatic brain injury: Pharmacotherapy options for cognitive deficits

Treatment of Catatonia With Methylphenidate in an Elderly Patient With Depression

Matthew L. Prowler, M.D., David Weiss, M.D., and Stanley N. Caroff, M.D.

Received June 2, 2008; revised July 1, 2008; accepted July 2, 2008. From the Dept. of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA; and the Philadelphia Veterans Affairs Medical Center. Send correspondence and reprint requests to Matthew L. Prowler, M.D., Dept. of Psychiatry, University of Pennsylvania School of Medicine, 3535 Market St., 2nd Fl., Philadelphia, PA 19104. e-mail: matthew.prowler@uphs.upenn.edu
© 2010 The Academy of Psychosomatic Medicine

BACKGROUND: Catatonia is especially common among patients with mood disorders. OBJECTIVE: The authors evaluated the effects of methylphenidate as an augmentation strategy in an elderly patient with catatonia and depression. METHOD: Methylphenidate was administered to a catatonic patient who had not responded to lorazepam. RESULTS: The patient showed an acute and marked response to methylphenidate. DISCUSSION: Methylphenidate may be effective as an adjunct in elderly depression patients with catatonia, as well as in medically ill, apathetic patients. However, there have been few attempts to study the role of psychostimulants in alleviating catatonia in general, or catatonia associated specifically with an underlying depressive disorder, even though catatonia is frequently associated with mood disorders.

Treatment of Catatonia With Methylphenidate in an Elderly Patient With Depression