What is the difference between keppra and lamictal

My school was effected, my work it was rediculous. What my doctor did was change my dose of Lamicatal because at the time I was only on mg 2x a day. Keppra though again is like speed. So you really have to take it everyday. If you don't OMG - it is at this point a dependancy for me. I have to really keep to a schedule. Topamax-tingles in my fingers.

Keppra- like speed, weight loss-able to keep it off. Which was a nice change all epilepsy meds I could never loose weight- I never really gain but never could loose. Lamictal- paranoia, loss of sleep and crazyness, memory loss. I saw this and I must say keppra sucks it landed me in the hospital for a long time I missed an entire semester of school. I've always been on lamictal since i was 9 and im 18 now it has worked for me they just put me on keppra because they wanted to see if it could work on me.

I've never taken Keppra, but I've heard a lot of nightmares about it. I am currently taking Lamictal. Not XR; just regular Lamictal. If you're not having the rash, Lamictal is safe.

About memory: they ALL cause loss of memory. Some people are affected more than others. Each brain is differentt. I take 4 AEDs, so we don't know which one s causes more memory loss.

My doctor claims it's an individual situation with every person. No one can be positive which drug causes more memory loss than the other.

As for how much is too much: Again, it's an individual situation. If you've gone over a month after completely stopping an AED, but still feel the side effects, call your neurologist.

Some drugs will have the same side effects. I hope you find Lamictal XR better. Keep a list of dates and times of all AED changes. Bring this to your neurologist each time you see her. I'm only 15 and after a couple of times I had my seizures, my neurologist put me on keppra, 2 times a day But I had the mood changes as for example like raging and maybe suicide thoughts.

Then my neurologist put me on lamictal For the first week of my transformation, I had to take 2 pills of keppra and half of lamictal, then for the second week I then started to take halves of keppra and lamictal.

After I took half of keppra and full of lamictal I think.. I'm not sure but on that third week of transformation I had a seizure, and I'm getting close a lot of having another one since I'm taking 2 lamictal each day.. I'm not sure if my body or organism is trying to get use to this medicine or.. I'm not sure. But I've only took keppra for about 2 or 3 months.

Before my siezures, I get like mini seizures where I'm awake but like I lose control of my arms where it's shaking upwards I'm not sure how to explain the shaking but it usually lasts like 5 seconds and it happens I think maybe every 3 minutes or so, but when I like go lay down on my side for a while it stops For participants 12 or older, advised daily doses were lamotrigine 50 mg morning and mg evening , levetiracetam mg twice per day, and zonisamide mg twice per day.

For children between 5 and 12, advised doses were lamotrigine 1. There were 37 deaths during the trial. The studies had several limitations, Marston and co-authors said. Seizure reports were collected through diaries and clinic visits, and some seizures may have been missed. Why does lamotrigine show a greater modulation at adjusted i.

There is little evidence at present to answer these questions. However, lamotrigine is often used as a mood stabilizer, in addition to being a broad spectrum anti-convulsant. This could be indicative of additional actions in the brain other than being solely thought of as a traditional sodium-channel blocker. In addition, the channels which showed N45 significant changes were located contralateral to the stimulated site, in line with the topographical modulation induced by positive modulators of GABAAR Premoli et al.

Future studies should assess whether lamotrigine-responsiveness i. In the non-invasive brain stimulation field, the choice of stimulation parameters such as intensity is of high relevance and it is crucial for the outcome of investigational and therapeutic studies Fitzgerald et al. It becomes even a more relevant challenge when targeting non-motor sites as it is difficult to disentangle excitability changes of the stimulated neural population. When designing experiments which include post-drug or post-intervention RMT measurements, it should be considered that RMT assessment can be time consuming and may affect the investigation of short-term after effect.

In this particular study, the effects of the two medications on cortical excitability lie in a wide time window appropriate for post-drug investigations.

It was shown that the effects of lamotrigine Tergau et al. To conclude, we show that the increased stimulation intensity determined a different mechanistic profile evaluated with TEPs.

Our results indicate that in future pharmaco-TMS-EEG experiments a range of stimulation intensities should be used in both pre- and post-drug conditions, in order to enable comparison of TEPs between conditions using relative vs. IP and MR contributed to the design and write-up. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

We wish to thank Ms. Rosie Jacobs, Ms. Sara Carlesso for help in data acquisition and Dr. Eugenio Abela for useful comments. Casula, E. Cattaneo, Z. Modulation of visual cortical excitability by working memory: effect of luminance contrast of mental imagery. Cheung, H. An in vitro investigation of the action of lamotrigine on neuronal voltage-activated sodium channels.

Epilepsy Res. Cunningham, M. The anticonvulsant, lamotrigine decreases spontaneous glutamate release but increases spontaneous GABA release in the rat entorhinal cortex in vitro.

Neuropharmacology 39, — Darmani, G. Epstein, C. Prolonged neurophysiologic effects of levetiracetam after oral administration in humans. Epilepsia 49, — Fecchio, M. The spectral features of EEG responses to transcranial magnetic stimulation of the primary motor cortex depend on the amplitude of the motor evoked potentials. Fitzgerald, P. Intensity-dependent effects of 1 Hz rTMS on human corticospinal excitability.

A comprehensive review of the effects of rTMS on motor cortical excitability and inhibition. Greenhill, S. The hazard ratio from the analysis of withdrawal rates was 2. The primary outcome measure was retention in the trial for 12 months. Methods used to evaluate efficacy included 1 percentage of patients seizure-free for 12 months, 2 time to first seizure, and 3 seizure-free retention rate. There were no significant differences between the 3 AEDs using any of the 3 methods.

Hence, these data suggested that the differences in retention were not due to differences in efficacy; in fact, the main limiting factor in patient retention was the occurrence of adverse drug reactions. Some have suggested that the carbamazepine dose was too high though dose adjustments were permitted in the Rowen et al study.

Initial, maintenance, and maximum dosages were 25 mg, mg, and mg per day for lamotrigine and mg, mg, and mg per day for carbamazepine, respectively. The primary end point was retention in the trial. This study used target dosages and titration rates similar to the UK trial by Brodie et al.

Our study confirms the findings reported in the head-to-head studies by Brodie et al 4 and Rowan et al 5 of better retention with newer AEDs such as lamotrigine. Our data also add to the available literature regarding the use of most other AEDs in older adults, as, to our knowledge, no prior comparison studies in this age group have included more than 3 AEDs.

The strength of our study is that we were able to compare rates of retention and seizure freedom for 10 commonly used AEDs, some new and some old, in the setting of routine clinical practice, while attempting to control for potential non-AED predictors of retention and seizure freedom and while stratifying our findings by severity of epilepsy. Some points must be kept in mind while interpreting our results. Higher retention rates do not necessarily mean better efficacy. Not everyone in our data set was seizure-free but many of them continued to take their AEDs even when they were not completely efficacious data not shown.

Therefore, retention rates may reflect tolerability more than efficacy. We attempted to account for potential patient-related factors that may have affected retention, but a logistic regression analysis was unable to identify any significant non-AED predictors.

Prior studies investigating clinical predictors of AED response have been inconclusive. Another major limitation of this study is the lack of reliable titration data for all AEDs.

We recognize that titration rate can have an important relationship with tolerability; in our database, titration rates were not consistently well documented and therefore were not analyzed. It is also likely that many patients were not examined by the treating physician at the time of the occurrence of an adverse effect, particularly when patients called in to report the occurrence of an adverse effect.

Despite the retrospective nature of this review, it is unlikely that important adverse effects would be underreported, since any adverse effect that is clinically significant or bothersome is likely to be reported by the patient on our intake questionnaires or noted by the physician.

These limitations reflect the situation in real-world clinical care, where imperfect reporting and recall bias is common. Furthermore, only 7. These results, and the fact that the mean times to intolerability were in the range of 3. There is evidence that older patients respond well to low or moderate doses of the first prescribed AED. There may be a potential bias in our retrospective sample if 1 or more of the AEDs tested were systematically used first. Our reporting of retention and seizure freedom in patients on the first newly started AED treatment supplementary Table 2 and supplementary Table 4 and the stratification of our analyses by refractoriness should compensate for this bias to some extent; in the analysis of patients newly started on their first AED, relative rates of retention and seizure freedom were similar to those of the overall group, though notably lamotrigine, levetiracetam, and carbamazepine were comparable in terms of retention and efficacy.

Another recent study reported outcomes in older patients median age, 73 years with newly diagnosed localization-related epilepsy whose AED treatment was begun at a single center over a year period. In summary, our retrospective, uncontrolled study suggests that lamotrigine and levetiracetam are more effective than most other AEDs in older patients with epilepsy.

Carbamazepine and gabapentin may have comparable effectiveness to lamotrigine and levetiracetam in newly diagnosed patients starting their first AED treatment. Valproate treatment appears to be effective in refractory cases. Oxcarbazepine was considerably less effective than other AEDs in our experience.