Why Persons With Epilepsy Don’t Take Their Medication?

In fact, over one-third fails to take their epilepsy medication at least 80% of the time. This is termed nonadherence and leads to high rates of morbidity and mortality.


Surprisingly, a single daily dose compared to 3 times a day improved adherence only from 57% to 65%. Depakote was taken least at 55% and Keppra most at 79%. This is unrelated to drug efficacy, and perhaps side effects were the cause.


Dr Paul Farmer, who established free medical clinics in Haiti and then went on to treat multidrug-resistant tuberculosis in Peru, said that noncompliance is the fault of the doctor, not the patient. If this is true, how can we improve compliance?


For patients, the main reason is forgetting, not depression, not denial. Warning patients about the risk of sudden death from a seizure and other intensive educational efforts seem to be of limited help. Simple memory aids seem better, such as associating doses with daily routines, using weekly pill boxes (very important), electronic pill bottle recording (not universally available), or setting alarms on smartphones. Pharmacies contacting physicians when medications are not refilled would also be helpful, but this would require extra time by the pharmacy and by the physician to contact the patient. According to Dr Edward Faught, who commented on the study, insurers should take this role because of potential cost savings.


Finally, giving patients “permission” to admit they do not take their medications consistently is critical. I would frame the question this way: “All my patients miss doses, how often do you?”


See Neurology, August 2, 2016, page 452-453 and page 466-472.


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Neurologists Should View MS In The Same Way That Rheumatologists View Rheumatoid Arthritis

The goal of treating rheumatoid arthritis has, in recent years, been a complete remission, i.e., cessation of disease activity. Neurologists seem much more cautious and risk-averse in treating multiple sclerosis.


Dr Gavin Giovannoni has been a forceful advocate of a different approach. He outlined this strategy at the 2016 AAN Annual Meeting.


His goal is to treat simultaneously all the pathogenic processes that underpin progressive MS. These strategies include:


  1. Anti-inflammatory therapies, which deal with both adaptive and innate immune responses.


  1. Neuroprotective therapies.


  1. Remyelination strategies.


Controlling the initial autoimmune-driven inflammatory component is key. Thereafter, neuroprotection should be sought for all stages of the disease. Lastly, remyelination medications fully improve recovery from relapses. They are less likely to lead to regaining lost function.


Further, he believes that aggressive treatment early in the disease is best. He views stem cell therapy as most effective and Lemtrada next for patients with poor prognostic factors and who have demonstrated an early aggressive course.


Neuroprotective therapies include sodium channel blockers, such as phenytoin, lamotrigine, riluzole, and oxcarbazepine; ion channel-1 blockers, such as amiloride; SSRIs, such as fluoxetine; phosphodiesterase inhibitors, such as ibudilast; microglial inhibitors, such as laquinimod and minocycline; and drugs that improve mitochondrial function, such as biotin and idebenone.


Regarding remyelination, there are 6 compounds in clinical trials. A monoclonal antibody to LINGO-1 is furthest along. Next is a retinoid X receptor agonist, then a muscarinic antagonist (benztropine). Also in trials is an antihistamine H3 antagonist, developed by GSK and termed clemastine; an anti-SEMA4D (VX15); and lastly biotin.


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Sleep Disorders In Parkinson’s

These sleep disorders in parkinson’s are mainly excessive daytime sleepiness, insomnia, rapid eye movement behavior disorder of sleep, and restless legs syndrome. Sleep can also be affected by nocturia, difficulty turning over in bed, hallucinations, dyskinesias, pain, dystonia.


How can we treat these symptoms? The best evidence is for using modafinil for excessive daytime sleepiness. Caffeine may be effective but with less robust evidence. The antidepressant doxepin may help insomnia. Rivastigmine may be effective for RDB of sleep, along with clonazepam, generally used first-line. Other studies show that stopping sedative medications and reducing dopamine agonists during the daytime help. Amoxetine, a “stimulating” antidepressant, could also help daytime sleepiness and would simultaneously be helpful for depression. Quetiapine and memantine do not help daytime sleepiness.


For insomnia, studies support use of doxepin, melatonin, eszopiclone. Nortriptyline but not paroxetine may also improve sleep quality, especially in patients with depression. Dopamine agonists have been long used to treat RLS and are FDA-approved to do so.


The most surprising new finding is that rivastigmine may help RBD, when it is refractory to clonazepam and melatonin. Less surprising is that modafinil helps daytime sleepiness.


See Parkinsonism & Related Disorders, 2016, page 25-34. Lead author is T.M. Rodrigues, MD.


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