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Comparative efficacy of phenytoin, steroid and carbamazepine in herpes zoster and post herpetic neuralgia
Agarwal S,Malhotra Y,Kalla G,Khullar R
Indian Journal of Dermatology, Venereology and Leprology , 1991,
Abstract: Three hundred patients of different ages were sequentially assigned three therapy groups (100 in each group) viz. phenytoin, steroid (prednisolone) and carbamazepine. Effect of these drugs on herpes zoster neuralgia and in prevention of post herpetic neuralgia was studied. Phenytoin was found to be superior to both steroid and carbamazepine in relieving the pain of herpes zoster and in reducing the incidence of post herpetic neuralgia. Only 16.1% of the patients in phenytoin treated group developed post herpetic neuralgia lasting for 2-4 weeks while 22.7% and 29.6% of the steroid and carbamazepine treated patients respectively developed post herpetic neuralgia and that too lasting for longer duration. No patient under 40 years developed post herpetic neuralgia.
Evaluating Aftereffects of Short-Duration Transcranial Random Noise Stimulation on Cortical Excitability  [PDF]
Leila Chaieb,Walter Paulus,Andrea Antal
Neural Plasticity , 2011, DOI: 10.1155/2011/105927
Abstract: A 10-minute application of highfrequency (100–640?Hz) transcranial random noise stimulation (tRNS) over the primary motor cortex (M1) increases baseline levels of cortical excitability, lasting around 1?hr poststimulation Terney et al. (2008). We have extended previous work demonstrating this effect by decreasing the stimulation duration to 4, 5, and 6 minutes to assess whether a shorter duration of tRNS can also induce a change in cortical excitability. Single-pulse monophasic transcranial magnetic stimulation (TMS) was used to measure baseline levels of cortical excitability before and after tRNS. A 5- and 6-minute tRNS application induced a significant facilitation. 4-minute tRNS produced no significant aftereffects on corticospinal excitability. Plastic after effects after tRNS on corticospinal excitability require a minimal stimulation duration of 5 minutes. However, the duration of the aftereffect of 5-min tRNS is very short compared to previous studies using tRNS. Developing different transcranial stimulation techniques may be fundamental in understanding how excitatory and inhibitory networks in the human brain can be modulated and how each technique can be optimised for a controlled and effective application. 1. Introduction Intermittent theta burst stimulation (iTBS) [1], high-frequency repetitive transcranial magnetic stimulation (rTMS) [2], anodal transcranial direct current stimulation (tDCS) [3], paired associative stimulation (PAS) [4], and now high-frequency random noise stimulation (tRNS) [5] are all techniques implemented in order to induce sustained elevations of cortical excitability, when applied over the primary motor cortex (M1). These methods of transiently modulating neuroplastic-like effects in the human cortex are generally short-lived, and dependent upon the stimulus duration and intensity. In the case of theta burst stimulation and anodal transcranial direct current stimulation, after effects are well characterised [3], and here we aim to evaluate the longer after effects observed poststimulation with high-frequency transcranial random noise (tRNS). The aim of this study was to investigate whether a threshold stimulation duration is necessary to produce sustained and measurable after effects on corticospinal excitability; a variable that has not been previously studied with regard to applications of tRNS. There is growing interest in understanding the effect of applying transcranial stimulation techniques in intervals of short-duration applications to optimise or prolong after effects; this has already been shown with tDCS
ATHEROSCLEROTIC RISK AMONG EPILEPTIC PATIENTS TAKING CARBAMAZEPINE, PHENYTOIN TREATMENT: BRIEF REVIEW  [PDF]
S. S. Khot*, Md. Hanif Shaikh and Lalitkumar Gupta
International Journal of Pharmaceutical Sciences and Research , 2013,
Abstract: ABSTRACT: Epilepsy is a common chronic neurological disorder that requires long-term or sometimes lifetime therapy. Anticonvulsant drugs are used in large quantities during long-term antiepileptic therapy and the treatment may be associated with various metabolic abnormalities in connective tissues, endocrine system and the liver. Recent evidence indicates that prolonged use of antiepileptic drugs (AEDs) particularly carbamazepine (CBZ), phenytoin (PHT) might modify some vascular risk factors; however, the influence of AED therapy on the development of atherosclerosis has been the subject of controversy and pretty unclear. Some epidemiological studies have reported a higher prevalence of ischemic vascular disease among epileptic patients on AEDs, while in other studies the mortality due to atherosclerosis-related cardiovascular disease in treated epileptics has been observed to be lower than in the general population. The etiology of atherosclerosis-related vascular diseases in epileptic patients has not been fully clarified. Atherosclerotic vascular alterations may start early in life, this review focuses on major atherogenic risk, including disordered lipid profiles, and increased lipoprotein (a) serum levels among epileptic patients.
Reversible onychomadesis induced by carbamazepine  [cached]
Prabhakara V,Krupa Shankar D
Indian Journal of Dermatology, Venereology and Leprology , 1996,
Abstract: An epileptic teenager put on carbamazepine therapy presented with onychomadesis 6 months later. Carbamazepine was substituted with phenytoin. Affected nails were shed and healthy nails regrew in 5 months.
Electrophysiological Analysis of Cortical Excitability and Inhibition Using Transcranial Magnetic Stimulation for Understanding Aggressive Behaviors in Antisocial Personality Disorder  [PDF]
Zülküf PERDEC?,Kamil Nahit ?ZMENLER,Erhan Ali DO?RUER,Fatih ?ZDA?
N?ropsikiyatri Ar?ivi , 2009,
Abstract: Objective: Some biological researches on aggressive behaviors suggest that cortical excitability and inhibition imbalance cause behavioral problems like reactive aggression, impulsivity and inability to behavioral control. The purpose of the study is to evaluate whether cortical excitability-inhibition imbalance is responsible for aggressive behaviors in adult young men with antisocial personality disorder in which aggressive behavior is one of the key features. Method: We studied 42 subjects with antisocial personality disorder and 44 healthy controls matched for age and education level. The electrophysiology of cortical inhibition and excitability was measured with transcranial magnetic stimulation. SCID-I, SCID-II, Aggression Questionnaire, and Edinburg Handedness Inventory were performed to all subjects. Results: Motor threshold, cortical latency, and central motor conduction time, which are related with cortical excitability, have been found statistically significant lower on antisocial personality disorder group compared with healthy controls. There was no difference between two groups on cortical silent period which reflects cortical inhibitory mechanisms. Conclusion: The results indicate an increase in cortical motor excitability on antisocial personality disorder, and we suggest that the cortical imbalance might render the person prone to behavior problems. (Archives of Neuropsychiatry 2009; 46: 44-8)
Transcranial Magnetic Stimulation for the treatment of tinnitus: Effects on cortical excitability
Berthold Langguth, Tobias Kleinjung, Joerg Marienhagen, Harald Binder, Philipp G Sand, G?ran Hajak, Peter Eichhammer
BMC Neuroscience , 2007, DOI: 10.1186/1471-2202-8-45
Abstract: We noted a significant interaction between treatment response and changes in motor cortex excitability during active rTMS. Specifically, clinical improvement was associated with an increase in intracortical inhibition, intracortical facilitation and a prolongation of the cortical silent period. These results indicate that intraindividual changes in cortical excitability may serve as a correlate of response to rTMS treatment.The observed alterations of cortical excitability suggest that low frequency rTMS may evoke long-term-depression like effects resulting in an improvement of subcortical inhibitory function.Subjective tinnitus is characterized by the perception of sound or noise in the absence of any internal or external acoustical stimulation. For 1–2% of the general population, this condition causes a considerable amount of distress and interferes seriously with the individual's ability to lead a normal life [1].The advent of modern neurophysiological and imaging tools has greatly benefited our understanding of the abnormal functioning of the central nervous system as a major cause of chronic tinnitus [2,3]. This is illustrated by a) an enhanced activation of the central auditory system in subjects suffering from tinnitus [4-7], b) the modulation of tinnitus perception by electrical stimulation of the auditory cortex [8,9] and c) changes in the tonotopic map of the auditory cortex visualized with magnetic source imaging [10,11]. These results have been complemented by evidence of dysfunctional thalamocortical processing in tinnitus [12-15]. Additional support for these findings comes from MRI studies demonstrating changes of thalamic structural plasticity in affected subjects [16]. Tinnitus-related hyperexcitability in specific brain regions along with dysfunctional neuroplasticity in critical cortical circuits have paved the way for addressing auditory phantom perceptions with rTMS based protocols: This method uses an electromagnet placed on the scalp that gene
Differential Modulation of Corticospinal Excitability by Different Current Densities of Anodal Transcranial Direct Current Stimulation  [PDF]
Andisheh Bastani, Shapour Jaberzadeh
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072254
Abstract: Background Novel non-invasive brain stimulation techniques such as transcranial direct current stimulation (tDCS) have been developed in recent years. TDCS-induced corticospinal excitability changes depend on two important factors current intensity and stimulation duration. Despite clinical success with existing tDCS parameters, optimal protocols are still not entirely set. Objective/hypothesis The current study aimed to investigate the effects of four different anodal tDCS (a-tDCS) current densities on corticospinal excitability. Methods Four current intensities of 0.3, 0.7, 1.4 and 2 mA resulting in current densities (CDs) of 0.013, 0.029, 0.058 and 0.083 mA/cm2 were applied on twelve right-handed (mean age 34.5±10.32 yrs) healthy individuals in different sessions at least 48 hours apart. a-tDCS was applied continuously for 10 minute, with constant active and reference electrode sizes of 24 and 35 cm2 respectively. The corticospinal excitability of the extensor carpi radialis muscle (ECR) was measured before and immediately after the intervention and at 10, 20 and 30 minutes thereafter. Results Post hoc comparisons showed significant differences in corticospinal excitability changes for CDs of 0.013 mA/cm2 and 0.029 mA/cm2 (P = 0.003). There were no significant differences between excitability changes for the 0.013 mA/cm2 and 0.058 mA/cm2 (P = 0.080) or 0.013 mA/cm2 and 0.083 mA/cm2 (P = 0.484) conditions. Conclusion This study found that a-tDCS with a current density of 0.013 mA/cm2 induces significantly larger corticospinal excitability changes than CDs of 0.029 mA/cm2. The implication is that might help to avoid applying unwanted amount of current to the cortical areas.
Transcranial magnetic stimulation provides means to assess cortical plasticity and excitability in humans with fragile X syndrome and autism spectrum disorder  [PDF]
Lindsay Oberman,Fritz Ifert-Miller,Umer Najib,Shahid Bashir,Ione Woollacott,Joseph Gonzalez-Heydrich,Jonathan Picker,Alexander Rotenberg,Alvaro Pascual-Leone
Frontiers in Synaptic Neuroscience , 2010, DOI: 10.3389/fnsyn.2010.00026
Abstract: Fragile X Syndrome (FXS) is the most common heritable cause of intellectual disability. In vitro electrophysiologic data from mouse models of FXS suggest that loss of fragile X mental retardation protein affects intracortical excitability and synaptic plasticity. Specifically, the cortex appears hyperexcitable, and use-dependent long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength are abnormal. Though animal models provide important information, FXS and other neurodevelopmental disorders are human diseases and as such translational research to evaluate cortical excitability and plasticity must be applied in the human. Transcranial magnetic stimulation paradigms have recently been developed to non-invasively investigate cortical excitability using paired pulse stimulation, as well as LTP- and LTD-like synaptic plasticity in response to theta burst stimulation (TBS) in vivo in the human. TBS applied on consecutive days can be used to measure metaplasticity (the ability of the synapse to undergo a second plastic change following a recent induction of plasticity). The current study investigated intracortical inhibition, plasticity and metaplasticity in full mutation females with FXS, participants with autism spectrum disorders (ASD), and neurotypical controls. Results suggest that intracortical inhibition is normal in participants with FXS, while plasticity and metaplasticity appear abnormal. ASD participants showed abnormalities in plasticity and metaplasticity, as well as heterogeneity in intracortical inhibition. Our findings highlight the utility of non-invasive neurophysiological measures to translate insights from animal models to humans with neurodevelopmental disorders, and thus provide direct confirmation of cortical dysfunction in patients with FXS and ASD.
Optimization of the Transcranial Magnetic Stimulation Protocol by Defining a Reliable Estimate for Corticospinal Excitability  [PDF]
Koen Cuypers, Herbert Thijs, Raf L. J. Meesen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086380
Abstract: The goal of this study was to optimize the transcranial magnetic stimulation (TMS) protocol for acquiring a reliable estimate of corticospinal excitability (CSE) using single-pulse TMS. Moreover, the minimal number of stimuli required to obtain a reliable estimate of CSE was investigated. In addition, the effect of two frequently used stimulation intensities [110% relative to the resting motor threshold (rMT) and 120% rMT] and gender was evaluated. Thirty-six healthy young subjects (18 males and 18 females) participated in a double-blind crossover procedure. They received 2 blocks of 40 consecutive TMS stimuli at either 110% rMT or 120% rMT in a randomized order. Based upon our data, we advise that at least 30 consecutive stimuli are required to obtain the most reliable estimate for CSE. Stimulation intensity and gender had no significant influence on CSE estimation. In addition, our results revealed that for subjects with a higher rMT, fewer consecutive stimuli were required to reach a stable estimate of CSE. The current findings can be used to optimize the design of similar TMS experiments.
Suppression of Motor Cortical Excitability in Anesthetized Rats by Low Frequency Repetitive Transcranial Magnetic Stimulation  [PDF]
Paul A. Muller, Sameer C. Dhamne, Andrew M. Vahabzadeh-Hagh, Alvaro Pascual-Leone, Frances E. Jensen, Alexander Rotenberg
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0091065
Abstract: Repetitive transcranial magnetic stimulation (rTMS) is a widely-used method for modulating cortical excitability in humans, by mechanisms thought to involve use-dependent synaptic plasticity. For example, when low frequency rTMS (LF rTMS) is applied over the motor cortex, in humans, it predictably leads to a suppression of the motor evoked potential (MEP), presumably reflecting long-term depression (LTD) – like mechanisms. Yet how closely such rTMS effects actually match LTD is unknown. We therefore sought to (1) reproduce cortico-spinal depression by LF rTMS in rats, (2) establish a reliable animal model for rTMS effects that may enable mechanistic studies, and (3) test whether LTD-like properties are evident in the rat LF rTMS setup. Lateralized MEPs were obtained from anesthetized Long-Evans rats. To test frequency-dependence of LF rTMS, rats underwent rTMS at one of three frequencies, 0.25, 0.5, or 1 Hz. We next tested the dependence of rTMS effects on N-methyl-D-aspartate glutamate receptor (NMDAR), by application of two NMDAR antagonists. We find that 1 Hz rTMS preferentially depresses unilateral MEP in rats, and that this LTD-like effect is blocked by NMDAR antagonists. These are the first electrophysiological data showing depression of cortical excitability following LF rTMS in rats, and the first to demonstrate dependence of this form of cortical plasticity on the NMDAR. We also note that our report is the first to show that the capacity for LTD-type cortical suppression by rTMS is present under barbiturate anesthesia, suggesting that future neuromodulatory rTMS applications under anesthesia may be considered.
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