Driving with Multiple Sclerosis: Can I? Should I?
Osteoporosis and Physical Activity Among NARCOMS ParticipantsNARCOMS Report–Symptomatic Medication and Cognitive Impairment in MS
Breanna Bullock, BA–NARCOMS Database Coordinator, Barrow Neurological Institute, Arizona.
Introduction
Cognitive deficits in multiple sclerosis (MS) are known to be a common feature of the disease. Presently, up to 65% of patients are affected (Bobholz & Rao, 2003; Amato, Portaccio, & Zipoli, 2006) and many report that they find the symptoms troublesome. It is well established that the dysfunction concerns a wide range of abilities. Anything from memory and processing speed to executive functions has been considered in neuropsychological studies (Bobholz & Rao, 2003). Prior to 1985 it was believed that, at most, 5% of patients with MS experienced cognitive problems and that they occurred only late in the course of the disease. More current research findings, however, indicate that the impairments can be detected in earlier stages and tend to continually progress over time (Amato, Ponziani, Siracusa, & Sorbi, 2001).
Various treatment approaches for cognitive impairments have been studied, but research continues to show mixed results.
Findings of some of these studies will be reviewed below. The primary goal of this paper, however, is to identify the proportion of NARCOMS Registry participants who report taking drugs known to affect cognition and to compare the self-reported level of cognitive deficit between those who are on these medications and those who are not.
Treatment of Cognitive Impairment
Although both pharmacological and nonpharmacological treatment regimens for cognitive impairment have been investigated, the majority of cognitive rehabilitation programs have focused on injury- rather than disease-induced impairment (Amato et al., 2006). Among patients with MS, the most promising therapies have been pharmacological in nature. Studies on beta-interferons (both 1a and 1b) and glatiramer acetate used as disease-modifying therapies have shown preliminary beneficial effects on cognition. It is suggested that their anti-inflammatory effects and protection against further tissue damage limit lesion activity and reduce the deterioration rate of brain tissue, thus slowing progression of cognitive dysfunction (Amato et al, 2006).
An article recently published by Dr. Barry Oken and his colleagues evaluated medications actively affecting neurotransmitters in the central nervous system (CNS) and their effects on cognitive function. The results of their study showed greater cognitive impairments in those patients taking these medications. Many of these CNS-active medications are commonly used by patients with MS.
NARCOMS Data
Upon enrollment and in all subsequent update surveys, NARCOMS participants report on the cognitive symptoms that they are experiencing. The measure used in the surveys is a six-point performance scale (PS) assessment ranging from Normal Cognition (0) to Total Cognitive Disability (5). The question refers to difficulty remembering, thinking, performing calculations, confusion, word recall, retaining information read, and so forth.
In addition to the PS question on cognition, the Spring 2005 update survey included a question addressing prescription medications other than those disease-modifying therapies specifically targeting MS. These medications and the proportion of participants reporting their use are listed in Table 1. The majority of these medications also appeared on Dr. Oken’s list of CNS -active drugs. Those not designated on the table as having been indicated in Dr. Oken’s study act as stimulants, but were not specifically referred to in his article.
Of the 9,531 participants who responded to the Spring 2005 survey, 6,157 (65%) reported using at least one of the listed drug therapies. Upon analyzing the cognitive PS scores for both those participants reporting taking CNS-active treatments and those not taking any, there was a clear difference between the two groups. The group reporting taking the CNS-active medications scored a disability level statistically significantly higher than those reporting not taking any of these drugs. This difference demonstrates the same indications as Dr. Oken’s findings. The CNS-active group tended to be older, but showed no differences between sexes. Basic participant information and average level of cognitive disability are listed in Table 2.
Conclusions
Dr. Oken and his colleagues investigated an important topic that inspired a similar analysis of the NARCOMS database. As a first step, we compared cognitive performance scale scores between patients treated with CNS-active drugs and those who were not treated with such drugs. While our initial findings do support those of Dr. Oken, the simple design does not allow us to conclude whether the drugs actually contribute to cognitive impairment. Analysis in much greater depth would be required to infer a causal relationship.
The Oken et al. article further suggested implications for future recruitment of study participants. The authors indicated that the effects of CNSactive medications on cognition may be evaluated as a potential interference when recruiting for clinical trials. However, since such a large number of patients with MS are frequently prescribed these medications, they concluded that it would be far too limiting to determine that anybody using these drugs should be excluded from clinical trials. In order to establish a more feasible recruitment strategy, this topic most certainly merits further investigation.
References
Amato, M. P., Ponziani, G., Siracusa, G., & Sorbi, S. (2001). Cognitive dysfunction in early-onset multiple sclerosis: A reappraisal after 10 years. Archives of Neurology, 58(10), 1602-6.
Amato, M. P., Portaccio, E., 7 Zipoli, V. (2006). Are there protective treatments for cognitive decline in MS? Journal of the Neurological Sciences, 245,183-6.
Bobholz, J. A., & Rao, S. M. (2003). Cognitive dysfunction in multiple sclerosis: A review of recent developments. Current Opinion in Neurology, 16, 283-8.
Gonzalez-Rosa, J. J., Vazquez-Marrufo, M., Vaquero, E., Duque, P., Borges, M., Gamero, M. A., et al. (2006). Differential cognitive impairment for diverse forms of multiple sclerosis. BMC Neuroscience, 7, 39.
Oken, B. S., Flegal, K., Zajdel, D., Kishiyama, S. S., Lovera, J., Bagert, et al. (2006). Cognition and fatigue in multiple sclerosis: Potential effects of medications with central nervous system activity. Journal of Rehabilitation Research & Development, 43(1), 83-90.
I started on Provigil almost a year ago, and I dearly LOVE it!! I had previously tried Ritalin, which worked for awhile, but the dosage kept having to be increased. Finally, my tolerance was just too high, and it was no longer effective for me. After researching Amantadine, it seemed that that particular drug had too many side-effects that would interfere with my bowel program and such. So on recommendation of the Mayo Clinic, I switched to Provigil.
So my main question: Is there anything currently in the works, or any way to try to get meds (like Provigil) re-classified as an MS drug? Now that I am on Medicare, I have had to enroll with a Medicare Part D company. I have had to fight and fight to get coverage for Provigil. The reason given by the Part D company is that “Provigil is not indicated for treatment of MS”. This is thoroughly frustrating!! How can this be remedied?