Background and purpose
This study aimed to assess the prevalence of illicit drug use among epilepsy patients and its effects on the disease.
Current treatments for depression and PTSD only suppress symptoms, if they work at all. What if we could prevent these diseases from developing altogether? Neuroscientist and TED Fellow Rebecca Brachman shares the story of her team’s accidental discovery of a new class of drug that, for the first time ever, could prevent the negative effects of stress — and boost a person’s ability to recover and grow. Learn how these resilience-enhancing drugs could change the way we treat mental illness.
This talk was presented at an official TED conference, and was featured by our editors on the home page.
Background: Pharmacological management of patients with epilepsy is still a very challenging approach for the best outcome of these patients. When considering the appropriate treatment choice for patients it is necessary to take into account several factors that can influence the effectiveness and quality of life. Cancelling or changing treatment suddenly can lead to uncontrolled seizures. After a short period without seizures, many patients are tempted to abandon treatment. Cessation of treatment can be discussed after a seizure-free period for at least two years. Treatment should be discontinued gradually by reducing the dosage and constant supervision of the physician. This paper analyses briefly the general pharmacological and treatment methods in several forms of adult epilepsy.
Conclusions: Management of epilepsy means more than observing the medication prescribed by the specialist. It is also important for the patient to maintain his general health status, monitor the symptoms of epilepsy and response to treatment and take care of his safety. Involvement in the management of one’s own affection can help the patient to control his condition and to continue his routine in usual manner. The objective of antiepileptic treatment is to reduce epileptic seizures to zero without intolerable side effects. New treatments should focus not only on reducing the frequency and intensity of seizures but also improving the quality of life of patients. Key words: patient, epilepsy, therapy and dynamics.
The analysis of the specialized literature reveals that many issues regarding differential treatment of epilepsy require subsequent clarification. As far as we are concerned, we have designed and developed therapeutic recommendations, in our opinion, effective, supporting the results of treating epilepsy in its various stages, from premonition to status variants. In this context, the main element in the choice of preparations, besides the trivial clinical signs, was the use of sub-curative monitoring data, including repeated EEG examinations, which fixed the subjective response of patients. Choosing the best possible medicine or an optimal combination of medicines is sometimes difficult. The perfect antiepileptic should be long, nonsedative, well tolerated, very active in various types of convulsive and with non-harmful effects on vital organs and functions. In addition, it must be effective in various forms of active epilepsy and in treating underlying epileptic seizures and capable of restoring the electroencephalogram between seizures to its normal form [5; 9; 10; 18; 23; 24; 27; 31; 38; 40; 41; 43].
It is still debatable whether such a drug will ever be discovered, and especially one that will control all types of epilepsy. The thorough study of pharmacological properties allows us to appreciate which of the existing antiepileptics will meet the current requirements of our patients under study. Due to the fact that patients differ considerably after clinical response to known anticonvulsants and the possibilities of treatment with associated drugs are insufficiently and superficially researched, testing of more efficient substances including new combinations continues. Due to the modern medication, which benefits from a wide and sufficiently efficient range of specific drugs, a large proportion of the recurrent and the disabling sequelae of the disease can be prevented. The adverse effects of drugs are low, so many of the past patients who have been labelled for life by this suffering can now live a productive life. The actual ability to control this disease effectively prevents more of its severe consequences [12; 13; 15; 22; 29; 46; 50].
General principles of pharmacotherapy of epilepsies
In the treatment of psychiatric disorders of our patients with epilepsy we have taken into account the following principles:
Appropriate selection of the remedy, its dosing, routes of administration and possible side effects. And we took into account the following:
of the evidence of side effects of favorable and unfavorable preparations. Somatic mood dictates and the route of administration of drugs: parenteral in gastrointestinal disorders, endonasal or transorbital (by electrophoresis) when parenteral administration is not preferred.
Individual features of the patient with epilepsy (age, weight, response to anticonvulsant therapy and others) are also considered. It is often forgotten that lower doses are indicated for children and older people as the exchange of substances in them is slow and standard dose treatment leads to accumulation of preparations and adverse effects [6; 7; 14; 19].
We recommend the gradual increase of the doses, with the preference of the minimal effective doses of the drugs. All the above-described drugs are initially indicated at minimal doses, then the dose gradually increases until the first positive effects are displayed, the subsequent increase of the doses is made after a certain period of time to stabilize the positive effect.
Complex treatment – it is necessary to prescribe unimoment of anticonvulsant remedies from different classes and groups in combination with non-medication methods. Polipharmacologic treatment has certain priorities in comparison with monotherapy because it addresses different links of the pathological process. It is important to avoid the multidimensional effects of many drugs, the doubling of the mechanisms of action and the predilection of some and the same psychological processes.
Continuous therapy. The treatment of productive disorders is done until their complete jugulation (sometimes with the purpose of preventing relapse and longer), of the deficient ones by alternating the cures, with gradual modifications [28; 30; 34; 39; 42].
Principles of medication of psychosomatic syndromes in epilepsy
Criteria for the effectiveness of psychotropic remedies administered in epilepsy are those of improving the knowledge and behavioral processes. More differentiated treatment is based on syndrome of mental disorders.
a) Main mechanism of action: nootrop, general metabolism, cerebrovascular or actoprotector;
b) Predominant action on mediating processes: GABA (piracetam, fenibut, gamma-aminobutyric acid); cholin-ergic (gliatiline); dopaminergic (nakom); and combined (meclofenoxate, glycine, glutamic acid);
c) With predominant action on the function of the encephalic structures: the cerebral and subcortical (nakom), on the left hemisphere (gliatilline); on the right hemisphere (cortexil);
d) With action on psychomotor activity: major stimulation (piracetam, nakom vinpocetine), mean enhancement (aminalone, gamma-aminobutyric acid, cerebrolizine, nicergoline, tanakan), diminishment (fenibut, glycine, ci-narizine);
e) Route of administration: parenteral, internal, endo-nasal, transorbital (by electrophoresis), mixed. Duration of treatment: from 7 days to 4 months (nakom, fenibut). On the basis of this therapy it is also possible to indicate prophylactic doses of anticonvulsants.
Emotional productive disruptions. In the states of excitation are indicated predominantly sedative neuroleptics and tranquilizers, antidepressants – in depression, tranquilizers and antiepileptics – in dysphoria, in anxiety states -neuroleptics and tranquilizers.
Productive districts nearby. Psychoparticular depressions are typically treated with “inor” euroleptics, preferably “behavioral correctors” or low doses of risperidone and tranquilizers; in neurotic manifestations (asthenia, obsessions, hysteria, hypocondria) are used tranquilizers and low doses of antidepressants [1; 2; 3; 4; 8; 11; 25; 26].
Continue —> SUPPORTIVE PRINCIPLES IN THE PHARMACOLOGICAL MANAGEMENT OF THE PATIENTS WITH EPILEPSY – тема научной статьи по медицине и здравоохранению читайте бесплатно текст научно-исследовательской работы в электронной библиотеке КиберЛенинка
My 54-year-old husband sustained a TBI when he fell asleep at the wheel while driving and hit a tree. The doctors say that he damaged all four parts of his brain. It’s been more than one and a half years and he’s still totally dependent on me to take care of him. Do you think Ritalin would help stimulate his brain?
Methylphenidate (Ritalin) is one of the commonly used brain stimulants in people who have suffered traumatic brain injury. It increases chemicals in the brain that have a stimulating effect (norepinephrine and dopamine).
After traumatic brain injury, doctors commonly prescribe Ritalin for low arousal or initiation, poor attention and concentration, depression, and slow processing speed. There is research that shows that Ritalin may speed recovery early after moderate to severe TBI. There is also research showing that Ritalin increases mental processing speed after TBI, which can improve memory function in some people.
All medications have side effects and the risks need to be weighed against possible benefits. One of the good things about the standard formulation of Ritalin is that it is short acting so if side effects occur they wear off in a few hours. Some potential side effects include keeping you up at night (if taken too close to bedtime), decreased appetite, headache, irritability, and paranoia.
In your husband’s case, his doctor needs to look at why he is so dependent. If arousal, attention, and/or initiation are playing a significant role, a stimulant can be considered. Careful monitoring for effects and/or side effects is needed when starting this medication and it should only be done by a doctor who has experience in caring for people with traumatic brain injury. Ritalin and most stimulants are controlled substances and will require frequent visits to the doctor for prescriptions.
To examine the effectiveness of levetiracetam and phenytoin for seizure prophylaxis following brain injury.
This study aimed to assess the prevalence of illicit drug use among epilepsy patients and its effects on the disease.
We systematically interviewed epilepsy outpatients at a tertiary epilepsy clinic. Predictors for active cannabis use were analysed with a logistic regression model.
Overall, 310 subjects were enrolled; 63 (20.3%) reported consuming cannabis after epilepsy was diagnosed, and 16 (5.2%) used other illicit drugs. Active cannabis use was predicted by sex (male) [odds ratio (OR) 5.342, 95% confidence interval (95% CI) 1.416–20.153] and age (OR 0.956, 95% CI 0.919–0.994). Cannabis consumption mostly did not affect epilepsy (84.1%). Seizure worsening was observed with frequent illicit (non-cannabis) drug use in 80% of cases.
Cannabis use does not seem to affect epilepsy; however, frequent use of other drugs increases seizure risk.
From May 20 to September 1 2014, Epilepsia conducted an online survey seeking opinions about the use of medical marijuana and cannabidiol (CBD) for people with epilepsy. This study reports the findings of that poll.
The survey consisted of eight questions. Four questions asked if there were sufficient safety and efficacy data, whether responders would advise trying medical marijuana in cases of severe refractory epilepsy, and if pharmacologic grade compounds containing CBD should be available. Four questions addressed occupation, geographic region of residence, if responders had read the paper, and if they were International League Against Epilepsy/International Bureau for Epilepsy (ILAE/IBE) members.
Of 776 who started or completed the survey, 58% were patients from North America, and 22% were epileptologists and general neurologists from Europe and North America. A minority of epileptologists and general neurologists said that there were sufficient safety (34%) and efficacy (28%) data, and 48% would advise using medical marijuana in severe cases of epilepsy. By comparison, nearly all patients and the public said there were sufficient safety (96%) and efficacy (95%) data, and 98% would recommend medical marijuana in cases of severe epilepsy. General physicians, basic researchers, nurses, and allied health professions sided more with patients, saying that there were sufficient safety (70%) and efficacy (71%) data, and 83% would advise using marijuana in severe cases. A majority (78%) said there should be pharmacologic grade compounds containing CBD, and there were no differences between specialists, general medical personal, and patients and the public.
This survey indicates that there is a wide disparity in opinion on the use of medical marijuana and CBD in the treatment of people with epilepsy, which varied substantially, with fewer medical specialists supporting its use compared with general medical personal, and patients and the public.
Continue —> Fewer specialists support using medical marijuana and CBD in treating epilepsy patients compared with other medical professionals and patients: Result of Epilepsia’s survey – Mathern – 2014 – Epilepsia – Wiley Online Library
BACKGROUND: Traumatic brain injury (TBI) is a major cause of chronic disability. Worldwide, it is the leading cause of disability in the under 40s, resulting in severe disability in some 150 to 200 million people per annum. In addition to mood and behavioural problems, cognition-particularly memory, attention and executive function-are commonly impaired by TBI. Cognitive problems following TBI are one of the most important factors in determining people’s subjective well-being and their quality of life. Drugs are widely used in an attempt to improve cognitive functions. Whilst cholinergic agents in TBI have been reviewed, there has not yet been a systematic review or meta-analysis of the effect on chronic cognitive problems of all centrally acting pharmacological agents.
OBJECTIVES: To assess the effects of centrally acting pharmacological agents for treatment of chronic cognitive impairment subsequent to traumatic brain injury in adults.
SEARCH METHODS: We searched ALOIS-the Cochrane Dementia and Cognitive Improvement Group’s Specialised Register-on 16 November 2013, 23 February 2013, 20 January 2014, and 30 December 2014 using the terms: traumatic OR TBI OR “brain injury” OR “brain injuries” OR TBIs OR “axonal injury” OR “axonal injuries”. ALOIS contains records of clinical trials identified from monthly searches of a number of major healthcare databases, numerous trial registries and grey literature sources. Supplementary searches were also performed in MEDLINE, EMBASE, PsycINFO, The Cochrane Library, CINAHL, LILACs, ClinicalTrials.gov, the World Health Organization (WHO) Portal (ICTRP) and Web of Science with conference proceedings.
SELECTION CRITERIA: We included randomised controlled trials (RCTs) assessing the effectiveness of any one centrally acting pharmacological agent that affects one or more of the main neurotransmitter systems in people with chronic traumatic brain injury; and there had to be a minimum of 12 months between the injury and entry into the trial.
DATA COLLECTION AND ANALYSIS: Two review authors examined titles and abstracts of citations obtained from the search. Relevant articles were retrieved for further assessment. A bibliographic search of relevant papers was conducted. We extracted data using a standardised tool, which included data on the incidence of adverse effects. Where necessary we requested additional unpublished data from study
authors. Risk of bias was assessed by a single author.
MAIN RESULTS: Only four studies met the criteria for inclusion, with a total of 274 participants. Four pharmacological agents were investigated: modafinil (51 participants); (-)-OSU6162, a monoamine stabiliser (12 participants of which six had a TBI); atomoxetine (60 participants); and rivastigmine (157 participants). A meta-analysis could not be performed due to the small number and heterogeneity of the studies.All studies examined cognitive performance, with the majority of the psychometric sub-tests showing no difference between treatment and placebo (n =
274, very low quality evidence). For (-)-OSU6162 modest superiority over placebo was demonstrated on three measures, but markedly inferior performance on another. Rivastigmine was better than placebo on one primary measure, and a single cognitive outcome in a secondary analysis of a subgroup with more severe memory impairment at baseline. The study of modafinil assessed clinical global improvement (n = 51, low quality evidence), and did not find any difference between treatment and placebo. Safety, as measured by adverse events, was reported by all studies (n = 274, very low quality evidence), with significantly
more nausea reported by participants who received rivastigmine compared to placebo. There were no other differences in safety between treatment and placebo. No studies reported any deaths.
AUTHORS’ CONCLUSIONS: There is insufficient evidence to determine whether pharmacological treatment is effective in chronic cognitive impairment in TBI. Whilst there is a positive finding for rivastigmine on one primary measure, all other primary measures were not better than placebo. The positive findings for (-)-OSU6162 are interpreted cautiously as the study was small (n = 6). For modafinil and atomoxetine no positive effects were found. All four drugs appear to be relatively well tolerated, although evidence is sparse.
Background: Several clinical studies have indicated that selective serotonin reuptake inhibitors (SSRIs) administered in patients after acute ischemic stroke can improve clinical recovery independently of depression. Due to small sample sizes and heterogeneous study designs interpretability was limited in these studies. The mechanisms of action whereby SSRI might improve recovery from acute ischemic stroke are not fully elucidated.
Methods: We searched MEDLINE using the PubMed interface to identify evidence of SSRI mediated improvement of recovery from acute ischemic stroke and reviewed the literature on the potential underlying mechanisms of action.
Results: Among identified clinical studies, a well-designed randomized, double-blind, and placebo-controlled study (FLAME – fluoxetine for motor recovery after acute ischemic stroke) demonstrated improved recovery of motor function in stroke patients receiving fluoxetine. The positive effects of SSRIs on stroke recovery were further supported by a meta-analysis of 52 trials in a total of 4060 participants published by the Cochrane collaboration. Based on animal models, the mechanisms whereby SSRIs might ameliorate functional and structural ischemic-brain damage were suggested to include stimulation of neurogenesis with migration of newly generated cells toward ischemic-brain regions, anti-inflammatory neuroprotection, improved regulation of cerebral blood flow, and modulation of the adrenergic neurohormonal system. However, to date, it remains speculative if and to what degree these mechanisms convert into humans and randomized controlled trials in large populations of stroke patients comparing different SSRIs are still lacking.
Conclusion: In addition to the need of comprehensive-clinical evidence, further elucidation of the beneficial mechanisms whereby SSRIs may improve structural and functional recovery from ischemic-brain damage is needed to form a basis for translation into clinical practice.
Continue —> Selective serotonin reuptake inhibitors to improve outcome in acute ischemic stroke: possible mechanisms and clinical evidence – Siepmann – 2015 – Brain and Behavior – Wiley Online Library
This is the protocol for a review and there is no abstract. The objectives are as follows:
To determine if pharmacological interventions for spasticity are more effective than no intervention, normal practice or control at improving function following stroke.
To determine if pharmacological interventions for spasticity after stroke are more effective than no intervention, normal practice or control at: