There is increasing evidence supporting dietary and alternative therapies for epilepsy, including the ketogenic diet, modified Atkins diet, and omega-3 fatty acids. Vitamin D is actively under investigation as a potential intervention for epilepsy. Vitamin D is fat soluble steroid which shows promise in animal models of epilepsy. Basic research has shed light on the possible mechanisms by which Vitamin D may reduce seizures, and animal data support the efficacy of Vitamin D in rat and mouse models of epilepsy. Very little clinical data exists to support the treatment of human epilepsy with Vitamin D, but positive findings from preliminary clinical trials warrant larger Phase I and II clinical trials in order to more rigorously determine the potential therapeutic value of Vitamin D as a treatment for human epilepsy.
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Background: Movement disorders in Huntington´s disease are often medically refractive. The aim of the trial was assessment of procedure safety of deep brain stimulation, equality of internal- and external-pallidal stimulation and efficacy followed-up for 6 months in a prospective pilot trial.Methods: In a conrolled double-blind phase 6 patients (4 chorea-dominant, 2 Westphal-variant) with predominant movement disorder were randomly assigned to either the sequence of 6 week internal-/6 week external-pallidal stimulation, or vice versa, followed by further 3 months chronic pallidal stimulation at the target with best effect-side-effect ratio. Primary endpoints were changes in the Unified Huntington´s Disease Rating Scale motor-score, chorea subscore and total motor-score 4 (blinded video ratings), comparing internal- versus external-pallidal stimulation, and 6 month versus baseline. Secondary endpoints assessed scores on dystonia, hypokinesia, cognition, mood, functionality/disability and quality-of-life. Results: Intention-to-treat analysis of all patients (n=3 in each treatment sequence): Both targets were equal in terms of efficacy. Chorea subscores decreased significantly over 6 months (-5.3 (60.2%), p=0.037). Effects on dystonia were not significant over the group due to it consisting of three responders (>50% improvement) and three non-responders. Westphal patients did not improve. Cognition was stable. Mood and some functionality/disability and quality-of-life scores improved significantly. 8 adverse events and 2 additional serious adverse events - mostly internal-pallidal stimulation-related - resolved without sequalae. No procedure-related complications occurred.Conclusion: Pallidal deep brain stimulation was demonstrated to be a safe treatment option for the reduction of chorea in Huntington´s disease. Their effects on chorea and dystonia and on quality-of-life, should be examined in larger controlled trials.
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Non-motor symptoms are now commonly recognized in Parkinson’s Disease (PD) and can include dysautonomia. Impairment of cardiovascular autonomic function can occur at any stage of PD but is typically prevalent in advanced stages or related to (anti-parkinsonian) drugs and can result in atypical blood pressure (BP) readings and related symptoms such as orthostatic hypotension (OH) and supine hypertension. OH is usually diagnosed with a head-up-tilt test (HUT) or an (active) standing test (also known as Schellong test) in the laboratory, but 24 hour Ambulatory Blood Pressure Monitoring (ABPM) in a home setting may have several advantages, such as providing an overview of symptoms in daily life alongside pathophysiology as well as assessment of treatment interventions. This, however, is only possible if ABPM is administrated correctly and an autonomic protocol (including a diary) is followed. which will be discussed in this review. A 24hr ABPM does not only allow the detection of OH, if it is present, but also the assessment of cardiovascular autonomic dysfunction during and after various daily stimuli, such as postprandial and alcohol dependent hypotension, as well as exercise and drug induced hypotension. Furthermore, information about the circadian rhythm of BP and heart rate (HR) can be obtained and establish whether or not a patient has a fall of BP at night (i.e. ‘dipper’ vs. non-‘dipper’). The information about nocturnal BP may also allow the investigation or detection of disorders such as sleep dysfunction, nocturnal movement disorders and obstructive sleep apnea, which are common in PD. Additionally, a 24hr ABPM should be conducted to examine the effectiveness of OH therapy. This review will outline the methodology of 24 hr ABPM in PD, summarize findings of such studies in PD and briefly consider common daily stimuli that might affect 24 Hr ABPM.
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Sudden infant death syndrome (SIDS) is an unexplained death in infants that usually occurs during sleep. The cause of SIDS remains unknown and multifactorial. In this regard, the diving reflex (DR), a peripheral subtype of trigeminocardiac reflex (TCR) is also hypothesized as one of the possible mechanisms for this condition. The TCR is a well-established neurogenic reflex which manifests as bradycardia, hypotension, apnea, and gastric hyper motility. The TCR shares many similarities with the DR which is a significant physiological adaptation to withstand hypoxia during apnea in many animal species including humans in clinical manifestation and mechanism of action. The DR is characterized by breath-holding (apnea), bradycardia and vasoconstriction leading to rising in blood pressure. Several studies have described congenital anomalies of autonomic nervous system in the pathogenesis of SIDS such as hypoplasia, delayed neuronal maturation or decreased neuronal density of arcuate nucleus, hypoplasia and neuronal immaturity of the hypoglossal nucleus. The abnormalities of autonomic nervous system in SIDS may explain the role of TCR in this syndrome involving sympathetic and parasympathetic nervous system. We reviewed the available literature to identify the role of TCR in the etiopathogenesis of SIDS and the pathways and cellular mechanism involved in it. This synthesis will help to update our knowledge and improve our understanding about this mysterious, yet common condition and will open the door for further research in this field.
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Obstructive sleep apnea is increasingly recognized as an important contributor to cognitive impairment, metabolic derangements and cardiovascular disease and mortality. Identifying the mechanisms by which this prevalent disorder influences health outcomes is now of utmost importance. As the prevalence of this disorder steadily increases, therapies are needed to prevent or reverse sleep apnea morbidities now more than ever before. Oxidative stress is implicated in cardiovascular morbidities of sleep apnea. What role oxidative stress plays in neural injury and cognitive impairments has been difficult to understand without readily accessible tissue to biopsy in persons with and without sleep apnea. An improved understanding of the role oxidative stress plays in neural injury in sleep apnea may be developed by integrating information gained examining neural tissue in animal models of sleep apnea with key features of redox biochemistry and clinical sleep apnea studies where extra-neuronal oxidative stress characterizations have been performed. Collectively, this information sets the stage for developing and testing novel therapeutic approaches to treat and prevent, not only central nervous system injury and dysfunction in sleep apnea, but also the cardiovascular and potentially metabolic conditions associated with this prevalent, disabling disorder.
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Antipsychotic-induced movement disorders are major side effects of antipsychotic drugs among schizophrenia patients, and include antipsychotic-induced parkinsonism (AIP) and tardive dyskinesia (TD). Substantial pharmacogenetic work has been done in this field, and several susceptibility variants have been suggested. In this paper, the genetics of antipsychotic-induced movement disorders is considered in a broader context. We hypothesize that genetic variants that are risk factors for AIP and TD may provide insights into the pathophysiology of Parkinson's disease (PD). Since loss of dopaminergic stimulation (albeit pharmacological in AIP and degenerative in PD) is shared by the two clinical entities, genes associated with susceptibility to AIP may be modifier genes that influence clinical expression of PD sub-phenotypes, such as age at onset, disease severity or rate of progression. This is due to their possible functional influence on compensatory mechanisms for striatal dopamine loss. Better compensatory potential might be beneficial at the early and later stages of the PD course. AIP vulnerability variants may also be related to latent impairment in the nigrostriatal pathway, affecting its functionality, and leading to subclinical dopaminergic deficits in the striatum. Susceptibility of PD patients to early development of L-dopa induced dyskinesia (LID), is an additional relevant sub-phenotype. LID may share a common genetic background with TD, with which it shares clinical features. Genetic risk variants may predispose to both phenotypes, exerting a pleiotropic effect. According to this hypothesis, elucidating the genetics of antipsychotic-induced movement disorders may advance our understanding of multiple aspects of PD and it clinical course, rendering this a potentially rewarding field of study.
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Postanoxic encephalopathy is the key determinant of death or disability after successful cardiopulmonary resuscitation. Animal studies have provided proof-of-principle evidence of efficacy of divergent classes of neuroprotective treatments to promote brain recovery. However, apart from targeted temperature management (TTM), neuroprotective treatments are not included in current care of patients with postanoxic encephalopathy after cardiac arrest. We aimed to review the clinical evidence of efficacy of neuroprotective strategies to improve recovery of comatose patients after cardiac arrest and to propose future directions. We performed a systematic search of the literature to identify prospective, comparative clinical trials on interventions to improve neurological outcome of comatose patients after cardiac arrest. We included 53 studies on 21 interventions. None showed unequivocal benefit. TTM at 33 or 36°C and adrenaline (epinephrine) are studied most, followed by xenon, erythropoietin, and calcium antagonists. Lack of efficacy is associated with heterogeneity of patient groups and limited specificity of outcome measures. Ongoing and future trials will benefit from systematic collection of measures of baseline encephalopathy and sufficiently powered predefined subgroup analyses. Outcome measurement should include comprehensive neuropsychological follow-up, to show treatment effects that are not detectable by gross measures of functional recovery. To enhance translation from animal models to patients, studies under experimental conditions should adhere to strict methodological and publication guidelines.
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Multiple sclerosis (MS) is a neurological disorder characterised by inflammatory demyelination and neurodegeneration in the central nervous system (CNS). Until recently, disease modifying treatment was based on agents requiring parenteral delivery, thus limiting long-term compliance. Basic treatments such as beta-interferon provide only moderate efficacy, and although therapies for second-line treatment and highly active MS are more effective, they are associated with potentially severe side effects. Fingolimod (Gilenya®) is the first oral treatment of MS and has recently been approved as single disease-modifying therapy in highly active relapsing-remitting multiple sclerosis (RRMS) for adult patients with high disease activity despite basic treatment (beta-interferon) and for treatment-naïve patients with rapidly evolving severe RRMS. At a scientific meeting that took place in Vienna on November 18th, 2011, experts from 10 Central and Eastern European countries discussed the clinical benefits and potential risks of fingolimod for MS, suggested how the new therapy fits within the current treatment algorithm and provided expert opinion for the selection and management of patients.
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Meniere’s disease and vestibular migraine are the most common causes of spontaneous recurrent vertigo. The current diagnostic criteria for the two disorders are mainly based on patients’ symptoms and no biological marker is available. When applying these criteria, an overlap of the two disorders is occasionally observed in clinical practice. Therefore, the present prospective multi-center study aimed to identify accompanying symptoms that may help to differentiate between Meniere’s disease (MD), vestibular migraine (VM) and probable vestibular migraine (pVM). Two hundred and sixty-eight patients were included in the study (MD: n = 119, VM: n = 84, pVM: n = 65). Patients with MD suffered mainly from accompanying auditory symptoms (tinnitus, fullness of ear and hearing loss), while accompanying migraine symptoms (migraine-type headache, photo-/phonophobia, visual aura), anxiety and palpitations were more common during attacks of VM. However, it has to be noted that a subset of MD patients also experienced (migraine-type) headache during the attacks. On the other hand, some VM/pVM patients reported accompanying auditory symptoms. The female/male ratio was statistically higher in VM/pVM as compared to MD, while the age of onset was significantly lower in the former two. The frequency of migraine-type headache was significantly higher in VM as compared to both pVM and MD. Accompanying headache of any type was observed in declining order in VM, pVM and MD. In conclusion, the present study confirms a considerable overlap of symptoms in MD, VM and pVM. In particular, we could not identify any highly specific symptom for one of the three entities. It is rather the combination of symptoms that should guide diagnostic reasoning. The identification of common symptom patterns in VM and MD may help to refine future diagnostic criteria for the two disorders.
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Correct function of neuronal networks is enabled by a delicate interplay among neurons communicating with each other. One of the keys is the communication at chemical synapses where neurotransmitters like glutamate, GABA and glycine enable signal transfer over the synaptic cleft. Thereby, the neurotransmitters are released from the presynapse and bind as ligands to specific receptors at the postsynaptic side to allow for modulation of the postsynaptic membrane potentials. The postsynaptic electrical signal, which is highly modulated by voltage gated ion channels, spreads over the dendritic tree and is thus integrated to allow for generation of action potentials at the axon hillock. This concert of receptors and voltage gated ion channels depends on correct function of all its components. Misfunction of receptors and/or voltage-gated potassium channels (VGKC) leads to diverse adverse effects in patients. Such malfunctions can be the result of inherited genetic alterations or pharmacological side effects by drugs. Recently, auto-antibodies targeting receptor or channel complexes like NMDAR, AMPAR, GABA-receptors, glycine-receptors, LGI1 or CASPR2 (previously termed VGKC-complex antibodies) have been discovered. The presence of specific auto-antibodies against these targets associates with severe forms of antibody-mediated encephalitis. Understanding the molecular details of auto-antibody actions on receptor and VGKC complexes is highly desirable and may open the path to develop specific therapies to treat humoral autoimmune encephalitis. Here, we summarize the current knowledge and discuss technical approaches to fill the gap of knowledge. These techniques include electrophysiology, biochemical approaches for epitope mapping and in silico modeling to simulate molecular interactions between autoantibody and its molecular target.
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There is increasing evidence supporting dietary and alternative therapies for epilepsy, including the ketogenic diet, modified Atkins diet, and omega-3 fatty acids. Vitamin D is actively under investigation as a potential intervention for epilepsy. Vitamin D is fat soluble steroid which shows promise in animal models of epilepsy. Basic research has shed light on the possible mechanisms by which Vitamin D may reduce seizures, and animal data support the efficacy of Vitamin D in rat and mouse models of epilepsy. Very little clinical data exists to support the treatment of human epilepsy with Vitamin D, but positive findings from preliminary clinical trials warrant larger Phase I and II clinical trials in order to more rigorously determine the potential therapeutic value of Vitamin D as a treatment for human epilepsy.
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Background: Movement disorders in Huntington´s disease are often medically refractive. The aim of the trial was assessment of procedure safety of deep brain stimulation, equality of internal- and external-pallidal stimulation and efficacy followed-up for 6 months in a prospective pilot trial.Methods: In a conrolled double-blind phase 6 patients (4 chorea-dominant, 2 Westphal-variant) with predominant movement disorder were randomly assigned to either the sequence of 6 week internal-/6 week external-pallidal stimulation, or vice versa, followed by further 3 months chronic pallidal stimulation at the target with best effect-side-effect ratio. Primary endpoints were changes in the Unified Huntington´s Disease Rating Scale motor-score, chorea subscore and total motor-score 4 (blinded video ratings), comparing internal- versus external-pallidal stimulation, and 6 month versus baseline. Secondary endpoints assessed scores on dystonia, hypokinesia, cognition, mood, functionality/disability and quality-of-life. Results: Intention-to-treat analysis of all patients (n=3 in each treatment sequence): Both targets were equal in terms of efficacy. Chorea subscores decreased significantly over 6 months (-5.3 (60.2%), p=0.037). Effects on dystonia were not significant over the group due to it consisting of three responders (>50% improvement) and three non-responders. Westphal patients did not improve. Cognition was stable. Mood and some functionality/disability and quality-of-life scores improved significantly. 8 adverse events and 2 additional serious adverse events - mostly internal-pallidal stimulation-related - resolved without sequalae. No procedure-related complications occurred.Conclusion: Pallidal deep brain stimulation was demonstrated to be a safe treatment option for the reduction of chorea in Huntington´s disease. Their effects on chorea and dystonia and on quality-of-life, should be examined in larger controlled trials.
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Non-motor symptoms are now commonly recognized in Parkinson’s Disease (PD) and can include dysautonomia. Impairment of cardiovascular autonomic function can occur at any stage of PD but is typically prevalent in advanced stages or related to (anti-parkinsonian) drugs and can result in atypical blood pressure (BP) readings and related symptoms such as orthostatic hypotension (OH) and supine hypertension. OH is usually diagnosed with a head-up-tilt test (HUT) or an (active) standing test (also known as Schellong test) in the laboratory, but 24 hour Ambulatory Blood Pressure Monitoring (ABPM) in a home setting may have several advantages, such as providing an overview of symptoms in daily life alongside pathophysiology as well as assessment of treatment interventions. This, however, is only possible if ABPM is administrated correctly and an autonomic protocol (including a diary) is followed. which will be discussed in this review. A 24hr ABPM does not only allow the detection of OH, if it is present, but also the assessment of cardiovascular autonomic dysfunction during and after various daily stimuli, such as postprandial and alcohol dependent hypotension, as well as exercise and drug induced hypotension. Furthermore, information about the circadian rhythm of BP and heart rate (HR) can be obtained and establish whether or not a patient has a fall of BP at night (i.e. ‘dipper’ vs. non-‘dipper’). The information about nocturnal BP may also allow the investigation or detection of disorders such as sleep dysfunction, nocturnal movement disorders and obstructive sleep apnea, which are common in PD. Additionally, a 24hr ABPM should be conducted to examine the effectiveness of OH therapy. This review will outline the methodology of 24 hr ABPM in PD, summarize findings of such studies in PD and briefly consider common daily stimuli that might affect 24 Hr ABPM.
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Sudden infant death syndrome (SIDS) is an unexplained death in infants that usually occurs during sleep. The cause of SIDS remains unknown and multifactorial. In this regard, the diving reflex (DR), a peripheral subtype of trigeminocardiac reflex (TCR) is also hypothesized as one of the possible mechanisms for this condition. The TCR is a well-established neurogenic reflex which manifests as bradycardia, hypotension, apnea, and gastric hyper motility. The TCR shares many similarities with the DR which is a significant physiological adaptation to withstand hypoxia during apnea in many animal species including humans in clinical manifestation and mechanism of action. The DR is characterized by breath-holding (apnea), bradycardia and vasoconstriction leading to rising in blood pressure. Several studies have described congenital anomalies of autonomic nervous system in the pathogenesis of SIDS such as hypoplasia, delayed neuronal maturation or decreased neuronal density of arcuate nucleus, hypoplasia and neuronal immaturity of the hypoglossal nucleus. The abnormalities of autonomic nervous system in SIDS may explain the role of TCR in this syndrome involving sympathetic and parasympathetic nervous system. We reviewed the available literature to identify the role of TCR in the etiopathogenesis of SIDS and the pathways and cellular mechanism involved in it. This synthesis will help to update our knowledge and improve our understanding about this mysterious, yet common condition and will open the door for further research in this field.
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Obstructive sleep apnea is increasingly recognized as an important contributor to cognitive impairment, metabolic derangements and cardiovascular disease and mortality. Identifying the mechanisms by which this prevalent disorder influences health outcomes is now of utmost importance. As the prevalence of this disorder steadily increases, therapies are needed to prevent or reverse sleep apnea morbidities now more than ever before. Oxidative stress is implicated in cardiovascular morbidities of sleep apnea. What role oxidative stress plays in neural injury and cognitive impairments has been difficult to understand without readily accessible tissue to biopsy in persons with and without sleep apnea. An improved understanding of the role oxidative stress plays in neural injury in sleep apnea may be developed by integrating information gained examining neural tissue in animal models of sleep apnea with key features of redox biochemistry and clinical sleep apnea studies where extra-neuronal oxidative stress characterizations have been performed. Collectively, this information sets the stage for developing and testing novel therapeutic approaches to treat and prevent, not only central nervous system injury and dysfunction in sleep apnea, but also the cardiovascular and potentially metabolic conditions associated with this prevalent, disabling disorder.
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Antipsychotic-induced movement disorders are major side effects of antipsychotic drugs among schizophrenia patients, and include antipsychotic-induced parkinsonism (AIP) and tardive dyskinesia (TD). Substantial pharmacogenetic work has been done in this field, and several susceptibility variants have been suggested. In this paper, the genetics of antipsychotic-induced movement disorders is considered in a broader context. We hypothesize that genetic variants that are risk factors for AIP and TD may provide insights into the pathophysiology of Parkinson's disease (PD). Since loss of dopaminergic stimulation (albeit pharmacological in AIP and degenerative in PD) is shared by the two clinical entities, genes associated with susceptibility to AIP may be modifier genes that influence clinical expression of PD sub-phenotypes, such as age at onset, disease severity or rate of progression. This is due to their possible functional influence on compensatory mechanisms for striatal dopamine loss. Better compensatory potential might be beneficial at the early and later stages of the PD course. AIP vulnerability variants may also be related to latent impairment in the nigrostriatal pathway, affecting its functionality, and leading to subclinical dopaminergic deficits in the striatum. Susceptibility of PD patients to early development of L-dopa induced dyskinesia (LID), is an additional relevant sub-phenotype. LID may share a common genetic background with TD, with which it shares clinical features. Genetic risk variants may predispose to both phenotypes, exerting a pleiotropic effect. According to this hypothesis, elucidating the genetics of antipsychotic-induced movement disorders may advance our understanding of multiple aspects of PD and it clinical course, rendering this a potentially rewarding field of study.
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Postanoxic encephalopathy is the key determinant of death or disability after successful cardiopulmonary resuscitation. Animal studies have provided proof-of-principle evidence of efficacy of divergent classes of neuroprotective treatments to promote brain recovery. However, apart from targeted temperature management (TTM), neuroprotective treatments are not included in current care of patients with postanoxic encephalopathy after cardiac arrest. We aimed to review the clinical evidence of efficacy of neuroprotective strategies to improve recovery of comatose patients after cardiac arrest and to propose future directions. We performed a systematic search of the literature to identify prospective, comparative clinical trials on interventions to improve neurological outcome of comatose patients after cardiac arrest. We included 53 studies on 21 interventions. None showed unequivocal benefit. TTM at 33 or 36°C and adrenaline (epinephrine) are studied most, followed by xenon, erythropoietin, and calcium antagonists. Lack of efficacy is associated with heterogeneity of patient groups and limited specificity of outcome measures. Ongoing and future trials will benefit from systematic collection of measures of baseline encephalopathy and sufficiently powered predefined subgroup analyses. Outcome measurement should include comprehensive neuropsychological follow-up, to show treatment effects that are not detectable by gross measures of functional recovery. To enhance translation from animal models to patients, studies under experimental conditions should adhere to strict methodological and publication guidelines.