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In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.
The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.
In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.
Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.
So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.
A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.
He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.
Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.
At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.
It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.
The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.
In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.
Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.
So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.
A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.
He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.
Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.
At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.
It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.
The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.
In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.
Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.
So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.
A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.
He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.
Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.
At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.
It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.