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Timothy L. Vollmer, MD
Department of Neurology
University of Colorado Health Sciences Center Professor

Co-Director of the RMMSC at Anschutz Medical Center

Medical Director-Rocky Mountain MS Center
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Brian R. Apatoff, MD, PhD
Multiple Sclerosis Institute
Center for Neurological Disorders

Associate Professor Neurology and Neuroscience,

Weill Medical College of Cornell University

Clinical Attending in Neurology,
New York-Presbyterian Hospital
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Timothy L. Vollmer M.D.
Department of Neurology
University of Colorado Health Sciences Center
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Woman with multiple sclerosis suing police over sobriety test

Times Herald-Record

MONTGOMERY — A woman suffering from multiple sclerosis is suing three Town of Montgomery police officers who gave her a sobriety test and arrested her in 2005, according to a case filed in U.S. District Court last week. Peggy Farganis, 34, claims Officers Dennis Barnett, Kenneth Byrnes and Daniel Thorson violated her civil rights when they arrested her on child endangerment charges and pursued civil action against her, according to the claim. Farganis was driving her son to the hospital after a fall when officers stopped her and questioned her sobriety. The woman claims her slightly slurred speech and disorientation is caused by her illness. Barnett gave Farganis a field sobriety test, which the claim says she failed because of stress heightening her symptoms.
Farganis was arrested and charged with endangering the welfare of a child. She was acquitted on Nov. 15, 2007, after a bench trial.

Former Village of Montgomery Officer-in-Charge Jack Byrnes was on the scene but is not named as a defendant in the suit. Farganis is asking for compensatory and punitive damages, lawyer's fees and other relief.

Montgomery police Chief Arnold "Butch" Amthor declined to comment on pending legislation. Lawyer Helen Ullrich, who represents the plaintiff, was unavailable for comment.



Emerging oral therapies for multiple sclerosis

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This review discusses the current unmet need for an orally administered treatment for RRMS, including potential benefits of this route of administration, and implications for improved treatment outcomes. Oral drugs that are currently in Phase II/III clinical development are discussed

Web-based literature review, focusing on studies investigating adherence to treatment for chronic diseases, plus information from clinical trials using named oral drugs (cladribine, teriflunomide, fingolimod, BG00012, laquinimod). These drugs were selected because they all met the criteria that data from at least Phase II level studies in relapsing MS had been published at the time the review was drafted...




Lilly to Acquire Exclusive Rights to Novel Late-Stage Molecule for the Treatment of MS

Lilly and BioMS Medical Announce Global Licensing and Development Agreement

Lilly to Acquire Exclusive Rights to Novel Late-Stage Molecule for the Treatment of Multiple

and BioMS Medical Corp. (TSX:MS) today announced that the two companies have entered into a licensing and development agreement granting Lilly exclusive worldwide rights to BioMS Medical's lead multiple sclerosis (MS) compound, MBP8298.

The compound is currently being
evaluated in two pivotal phase III clinical trials in secondary progressive MS (SPMS) and one
phase II clinical trial in relapsing-remitting MS (RRMS).

Under the terms of the agreement, Lilly and BioMS Medical will collaborate on the development
of MBP8298 and will also share in certain development costs with Lilly being responsible for
future R&D, manufacturing and marketing activities. BioMS Medical will receive an upfront
payment of $87 million, as well as potential development and sales milestones up to $410
million and escalating royalties on sales commensurate with the current stage of development of
the product if MBP8298 is successfully commercialized. BioMS Medical will continue to
oversee the current clinical trials. Other terms of the deal were not disclosed.

"Lilly is pleased to add yet another promising late-stage compound to our portfolio,” said Dr.
William W. Chin, M.D., vice president of discovery research and clinical investigation for Lilly.
"Multiple sclerosis is a disease with significant unmet patient needs. MBP8298 has shown
potential in slowing the progression of secondary progressive MS, and thus may provide an
effective therapeutic option for patients with this debilitating disease. We are also hopeful that

MBP8298 may prove beneficial in treating patients with relapsing remitting MS. We intend to
fully leverage our expertise in neuroscience to continue the development of this novel molecule."

“We are very pleased to collaborate with Lilly on the worldwide development of MBP8298,”
said Kevin Giese, President and CEO at BioMS Medical. “Lilly’s well established leadership in
the neurology arena and considerable resources, expertise and proven ability to launch first-in-
class drugs will help MBP8298 to realize its full development and commercial potential.”

The transaction is expected to become effective in the first quarter of 2008, contingent upon
clearance under the Hart-Scott-Rodino Anti-Trust Improvements Act, if required. At closing,
Lilly would expect a charge to earnings for acquired in-process research and development. The
exact amount of the charge has not yet been determined, but is estimated to be $0.05 per share.

About MBP8298
MBP8298 is a synthetic peptide that consists of 17 amino acids having a sequence identical to
that of a portion of human myelin basic protein (MBP). MBP8298 is being developed for the
potential treatment of multiple sclerosis (MS), an autoimmune disease caused by immune attack
against normal components of the central nervous system. The sequence of MBP8298 is
associated with the autoimmune process in MS patients with certain immune response genes
(HLA types DR2 and/or DR4); MS patients having these genes represent 65 to 75 percent of all
MS patients.

The apparent mechanism of action of MBP8298 is the induction or restoration of immunological
tolerance with respect to ongoing immune attack as a result of high doses of peptide delivered
periodically by the intravenous route. The potential benefit of MBP8298 for any individual
patient is therefore expected to be related to the role this peptide plays in that patient’s immune
system. The degree of immunomodulation achieved will depend on the relationship among the
peptide, HLA molecules and T cells.

The results of phase II and long-term follow-up treatment of MS patients with MBP8298,
published in 2006 in the European Journal of Neurology (EJN), showed that MBP8298 safely
delayed median time to disease progression for five years (versus placebo) in progressive MS
patients with HLA types DR2 and/or DR4. Thus, MBP8298 has the potential to be used as a
tailored therapy for patients genetically determined to express the appropriate HLA molecules.

MBP8298 is being developed in three late-stage clinical trials:
- MAESTRO-01: A pivotal phase II/III trial for secondary progressive MS (SPMS)
patients in Canada and Europe.
- MAESTRO-03: A pivotal phase III trial for SPMS patients in the United States.
- MINDSET-01: A phase II trial for relapsing-remitting MS (RRMS) patients in Europe.



"Cannabinoid system and neuroinflammation: implications for multiple sclerosis"


Cannabinoid system and neuroinflammation:

implications for multiple sclerosis

There is a growing amount of evidence suggesting that cannabinoids may be neuroprotective in central nervous system inflammatory conditions.
Advances in the understanding of the physiology and pharmacology of the cannabinoid system have potentiated the interest in cannabinoids as potential therapeutic targets. Here our aim was to update the actions of cannabinoids on immune system and glial cells and their implications on multiple sclerosis. We also show our results on the modulation of cytokines of the IL-12 family by cannabinoids in macrophages and brain microglia.

We used murine primary cultures of macrophage and microglia activated by lipopolysaccharide/IFN-gamma and Theiler's virus to study the effects of cannabinoids on the regulation of IL-12 and IL-23 mRNA and protein IL-12p40, evaluated by RT-PCR and ELISA, respectively. Cannabinoids negatively regulate the production of these cytokines by microglial cells in part due to the activation of CB(2) receptors.

The effects of cannabinoids on cytokine brain work and on the regulation of neuroinflammatory processes may affect chronic inflammatory demyelinating diseases such as multiple sclerosis.

Copyright (c) 2007 S. Karger AG, Basel.PMID: 18073512 [PubMed - in process]



Current Research on Existing and Emerging Therapies for the Treatment of MS

Current Research on Existing and Emerging Therapies for the Treatment of MS


ECTRIMS 2007: 23rd Congress of the European Committee for Treatment and Research in Multiple Sclerosis


The ECTRIMS 2007: 23rd Congress of the European Committee for Treatment and Research in Multiple Sclerosis, held in Prague, Czech Republic, from October 11 to 14, 2007, discussed the current research and treatment in multiple sclerosis (MS). Scientists and clinicians addressed key issues in the pathogenesis, diagnosis, and treatment of MS. Currently, there are 6 US Food and Drug Administration (FDA)-approved disease-modifying treatments: interferon beta-1a (intramuscular or subcutaneous), interferon beta-1b, glatiramer acetate, mitoxantrone, and natalizumab. This summary discusses the new data presented about these current treatment options and new potential treatments for MS.

New Treatments in Development

Daclizumab, a treatment for renal allograft transplant, is a humanized anti-CD25 monoclonal antibody that blocks the alpha chain of the interleukin-2 receptor. In the CHOICE trial, 230 actively relapsing patients on interferon beta were randomized to treatment with either placebo or 1 mg/kg or 2 mg/kg of daclizumab subcutaneously every 2 weeks for 24 weeks. The mean number of new or enlarging contrast-enhancing lesions at weeks 8-24 were 72% reduced in the 2-mg/kg treated arm compared with placebo (P = .004). A 25% reduction in enhancing lesions was seen on the lower dose, but was not statistically significant. Relapse rate reduction was 33% on the high dose, but was not statistically significant. Serious infections were more common in the patients who were treated with the higher dose, which was reported by Montalban and colleagues.[1]

FTY720 (fingolimod), an important potential oral treatment for MS, is in multiple phase 3 clinical trials. As a potent agonist on sphingosine 1-phosphate (S1P) receptors, FTY720 prevents the egress of activated lymphocytes from peripheral lymphoid tissue. Because S1P receptors are also expressed on astrocytes, oligodendrocytes, microglia, and neurons, other potential mechanisms of action are being explored in new research. FTY720 in cell culture studies has been shown to increase both mature and immature oligodendrocyte lineages, raising the possibility of remyelination.[2] Intraventricular administration of FTY720 reduced the degree of experimental allergic encephalomyelitis (EAE) without decreasing the peripheral lymphocyte count.[3] S1P receptor type 1 knockout mice developed attenuated EAE independent of FTY720 administration.[4]

BHT-3009 is a DNA plasmid vaccine that encodes the full-length myelin basic protein. In a phase 2b trial, 289 patients were randomized to placebo, 0.5 mg of BHT-3009 intramuscular injections, or 1.5 mg of BHT-3009 intramuscular injections. The median rate of contrast-enhancing lesions between weeks 24 and 28 was reduced 50% on the 0.5-mg BHT-3009 dose (P = .07). The 1.5-mg BHT-3009 has no significant effect on contrast-enhancing lesions. In addition, no significant effect was seen either on the relapse rate or T2 lesions, as described in the oral presentation by Garren and colleagues.[5]

MN-166 (ibudilast) is an oral agent with anti-inflammatory and neuroprotectant properties. Two hundred ninety-seven relapsing patients were randomized to placebo, 30 mg/day or 60 mg/day. More patients were relapse-free on 60 mg than on placebo (56.1% vs 41.0%, P = .03). In addition, time to first relapse was greater than 1 year on MN-166 60 mg/day and 244 days on placebo (P = .04). A lower mean cumulative active lesion count was seen on 60 mg/day compared with placebo, but this primary endpoint result was not statistically significant. MN-166 60 mg/day did significantly attenuate the percentage of brain volume loss (P = .04).[6]

Fluoxetine may have beneficial effects in MS because it can reduce lymphocyte proliferation, suppress interferon-gamma, and increase production of neurotrophic factors. Forty relapsing nondepressed patients were randomized to 20 mg of fluoxetine daily or placebo. The mean cumulative number of enhancing lesions during the 24 weeks of treatment was 1.84 on fluoxetine and 5.16 on placebo (P = .15). A significantly lower number of scans had new enhancing lesions on fluoxetine than on placebo (25% vs 41%; P = .04).[7]

Updates on Existing Treatments

The Rebif vs Glatiramer Acetate in Relapsing MS Disease (REGARD) trial examined the efficacy and safety of interferon beta-1a 44 micrograms (mcg) subcutaneously thrice weekly and glatiramer acetate in a randomized assessor-blind trial of 764 patients over 96 weeks. The time to the first relapse for the 30th percentile of patients was 495 days on interferon beta-1a and 432 days on glatiramer acetate. This primary endpoint measure was not statistically significant (P = .643). In the prespecified subgroup analysis of the patients with a score less than or equal to the median Expanded Disability Status Scale (EDSS), a significant difference was seen in the primary outcome measure (P = .022). The overall on-treatment annualized relapse rate was only 0.3, which was much less than planned to demonstrate a 30% difference between the 2 treatments on time to first relapse.

The number of lesions per patient per scan for interferon beta-1a and glatiramer acetate, respectively, was 0.7 vs 0.8 for T2-active lesions (P = .178), 0.2 vs 0.4 for T1-enhancing lesions (P < .001), and 0.9 vs 1.2 for combined unique lesions (P = .010).[8] The effect on T2-active lesions was not statistically significant, but the benefit of interferon beta-1a on T1-enhancing lesions was significant. A similar number of adverse events were seen with both treatments. Discontinuations due to adverse events were 8.1 % on interferon beta-1a (1.6% for flulike symptoms) and 6.4% on glatiramer acetate (1.3% for immediate postinjection reactions). At last assessment at 96 weeks, 27.3% of the patients were neutralizing antibody-positive on interferon therapy.[9]

The BECOME trial is a single-center, 2-year study of 75 patients randomized to interferon beta-1b or glatiramer acetate. The confirmed annualized relapse rate was 0.28 on interferon and 0.32 on glatiramer acetate, which was not statistically significant (P = .80). No difference was seen on the EDSS or Multiple Sclerosis Functional Composite (MFSC).[10] The median number of combined active lesions over 24 months was 0.60 on interferon and 0.38 on glatiramer acetate, which was also not statistically significant (P = .24). The median reduction in contrast-enhancing lesions from baseline to on-treatment was 1.19 on interferon beta-1b (P < .001) and 0 on glatiramer acetate (P = .14), which statistically favored interferon beta-1b treatment.[11]

Interferon beta-1a (new formulation) 96-week data revealed a last observation prevalence of neutralizing antibodies of 17%. This preparation of interferon beta-1a lacks human serum albumin. The injection site reactions were only 30.8% compared with 85.8% in the EVIDENCE trial.[12] The COGIMUS trial interim 2-year data demonstrated a significant dose-dependent benefit of interferon beta-1a thrice weekly subcutaneously on neuropsychological testing. Twenty-eight percent of patients on 44 mcg and 39% of patients on 22 mcg had impairment in at least 2 cognitive tests (P = .035).[13]

Further analysis of the BENEFIT trial elucidated the role of interferon beta-1b in patients treated with clinically isolated syndrome. Treatment initiation after the first attack reduced the risk for confirmed EDSS progression by 40% compared with delayed treatment (P = .022). In the early treatment group, 31.8% of patients were neutralizing antibody-positive at any time over 3 years, but 46.6% became antibody-negative by 3 years. Neutralizing antibody positivity did not affect the time to clinically definite MS or time to confirmed disability progression.[14] On the basis of 393 patient MRI studies from the European secondary progressive trial, cerebral brain volume dropped significantly more on interferon beta-1b than placebo on the first year of treatment and less than placebo from years 1 to 3.[15]

Several glatiramer-specific T-cell lines were generated from the cerebrospinal fluid of glatiramer acetate-treated MS patients. Eleven out of 12 of the T-cell lines were of the TH2 phenotype and secreted brain-derived neurotrophic factor.[16]

The STRATA study is examining redosing of natalizumab in patients who participated in the AFFIRM, SENTINEL, and GLANCE trials after voluntary suspension of natalizumab. Of the 1076 patients, 40 (3.7%) developed hypersensitivity reactions. These reactions occurred most frequently in those patients receiving only 1 or 2 doses prior to redosing. No new cases of progressive multifocal leukoencephalopathy have been reported.[17] Khatri and colleagues[18] demonstrated that plasma exchange reduced the serum concentration of natalizumab, which potentially could be a strategy to help restore immunocompetence if progressive multifocal leukoencephalopathy occurs. Interim data of an ongoing trial demonstrated statistically significant improvement on the Fatigue Severity Scale and the Modified Fatigue Impact Scale in 19 patients treated with natalizumab. In addition, improvement was also seen in Beck's Depression Inventory.[19] Oral treatment with a different alpha-4 integrin-blocking agent, AJM300, was effective in reducing the severity of EAE in the Lewis rat.[20]

Combination or Induction Therapy

Mitoxantrone induction therapy followed by interferon beta-1b was compared with interferon beta-1b therapy alone over 3 years in 109 active MS patients. The induction protocol consisted of methylprednisolone 1 g and mitoxantrone 20-mg monthly infusions for 6 months. Nine percent of induction-treated patients and 26% of interferon-only patients had worsening disability of greater than 1 EDSS point (65% benefit). The annualized relapse rate with induction was 0.44 compared with 1.14 on interferon only (56% benefit; P < .007).[21] The risks for mitoxantrone were highlighted in a study in Spain that calculated a leukemia incidence of 2.83% (95% confidence interval 1.2-4.4) in exposed patients.[22] This rate was much higher than previously recorded, including the 0.25% prevalence in a French cohort of 802 patients.[23]

Use of statin medications in MS was reexamined. An earlier pilot trial had demonstrated increased relapses and MRI-enhancing lesions on the combination of atorvastatin (40 or 80 mg) and interferon beta-1a subcutaneously.[24] In a separate randomized trial in Naples, Italy, using only 20 mg of atorvastatin, no significant differences were seen with combination therapy. Twenty-eight percent of patients on interferon beta-1a subcutaneously thrice weekly and 25% of patients on both interferon beta-1a and atorvastatin 20 mg daily had MRI-enhancing lesions.[25] Interim safety analysis of 47 patients in the SIMCOMBIN trial on 80 mg of simvastatin or placebo in addition to interferon beta-1a 30 mcg intramuscularly demonstrated no antagonistic effects of the combination therapy.[26] In a pilot study with MRI imaging, 12 clinically isolated syndrome patients were randomized to placebo or simvastatin 80 mg daily plus interferon beta-1a intramuscularly. The addition of simvastatin was safe and well tolerated.[27]

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Antidepressants: Selecting one that's right for you - MAYO CLINIC

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Antidepressants: Selecting one that's right for you

Daunted by the choice in antidepressants? With persistence, you and your doctor should find one that works so you can enjoy life more fully again.

Antidepressant medications are often the first treatment choice for adults with moderate or severe depression, sometimes along with psychotherapy. Although antidepressants may not cure depression, they can help you achieve remission — the disappearance or nearly complete reduction of depression symptoms.

With scores of antidepressants available, finding the right medication for your situation can be challenging, though. Explore the decision-making process that may help you and your doctor find the best antidepressant for your situation.

Finding the right antidepressant for you

Finding the right antidepressant for your situation might take time. Each antidepressant has its own pros and cons, and until you try one, you won't know exactly how it'll affect you or how well it'll work. You may need to try several antidepressants before finding the one, or the combination, that works best for you.

In general, most antidepressants work pretty well for most people. So which antidepressant you and your doctor choose depends largely on:

Anticipated side effects

Your ability to tolerate these side effects and stick with the treatment
Cost and health insurance coverage
Previous experiences you or family members have had with antidepressants
Whether you're pregnant or breast-feeding
Your age
Your other medical and psychiatric conditions

Blood test may help in choosing antidepressants

A blood test may help make the antidepressant decision somewhat easier. The test, called the cytochrome P450, helps pinpoint genetic factors that influence your response to certain antidepressants (as well as some other medications). The test doesn't predict which antidepressant will work best for you. But it does help suggest which ones may not work, and which ones may have the greatest side effects specifically for you.

Antidepressants: Test shows which may be your best bet

Approach to antidepressant treatment
Antidepressants are generally prescribed in a step-by-step treatment approach. When you're beginning treatment for the first time, doctors typically start by prescribing a type of antidepressant that's thought to be very effective and has the fewest side effects. If this doesn't work, your doctor may prescribe different types of antidepressants or combinations of two or more antidepressants and other medications. Don't give up until you find an antidepressant that's suitable for you — you have a good chance of finding one that works and doesn't have intolerable side effects.

First choices in antidepressants
Many doctors start by prescribing antidepressants known as SSRIs — selective serotonin reuptake inhibitors. This is because the side effects of these kinds of antidepressants are generally more tolerable than those of other types of antidepressants, and they also generally work well.

Other common first choices include:
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
Norepinephrine and dopamine reuptake inhibitors (NDRIs)
Combined reuptake inhibitors and receptor blockers
Tetracyclic antidepressants

Second choices in antidepressants

The class of antidepressants called tricyclic antidepressants (TCAs) has been around longer than SSRIs, but TCAs are still effective. However, because TCAs tend to have more numerous and more severe side effects, they're often not used until you've tried SSRIs first without an improvement in your depression.

Last choices in antidepressants
The type of antidepressants called monoamine oxidase inhibitors (MAOIs) is often used as a last resort, when other medications haven't worked. That's because MAOIs can have serious side effects and require strict dietary restrictions because of rare but potentially fatal interactions. However, MAOIs can be very effective for some forms of depression. And newer versions of MAOIs that you stick on your skin as a skin patch rather than swallowing may have fewer side effects.

Trying out antidepressants
Once you and your doctor have selected an antidepressant — whether you start with a first, second or last choice — it may take four to eight weeks for it to be fully effective in controlling your depression symptoms. In rare cases, it may take 12 to 14 weeks to achieve the full effects of an antidepressant. And with some medications, you can take the full dosage immediately. With others, you may need to gradually increase your dose. Talk to your doctor or therapist about coping with depression symptoms as you wait for medications to take effect.

If you have no significant improvement in your symptoms after six weeks, talk to your doctor about trying a different antidepressant or adding a second antidepressant or another medication. A medication combination may work better for you than does a single antidepressant.

You may have to taper off one medication before starting another. This is because potentially dangerous medication interactions, such as serotonin syndrome, and withdrawal-like symptoms can occur from an abrupt switch.

In rare cases, antidepressants simply might not work for you. You may need to consider other forms of treatment.

Side effects of antidepressants
All antidepressants can cause unwanted side effects. Not everyone experiences the same number or intensity of side effects, though. You may find that your side effects are so mild that you don't need to stop taking the antidepressant. Coping strategies also can help you manage side effects. In addition, side effects often go away or lessen within several weeks of starting an antidepressant.

If you experience unpleasant or intolerable side effects, don't just stop taking an antidepressant without consulting your doctor first. Some antidepressants can cause withdrawal-like symptoms unless you slowly taper off your dose.

Some antidepressants have the potential of causing serious or even life-threatening problems, such as liver failure or a dangerous drop in white cell count. While such cases are rare, it's important to get blood work or other tests on schedule and stick to your treatment regimen.

Antidepressants: Get tips to cope with side effects

Precautions when taking antidepressants

Although studies have shown that antidepressants are generally safe, some precautions are in order when taking them. The Food and Drug Administration (FDA) now requires that all antidepressant medications carry black box warnings. These are the strictest warnings that the FDA can issue for prescription medications.

The antidepressant warnings note that in some cases, children, adolescents and young adults ages 18 to 24 may have an increase in suicidal thoughts or behavior when taking antidepressants, especially in the first few weeks after starting an antidepressant or changing a dosage. Because of this risk, they must be closely monitored by loved ones, caregivers and health care providers while taking antidepressants.

In addition, if you're pregnant or breast-feeding, some antidepressants may pose an increased health risk to your unborn child. Talk to your doctor about any concerns you have, and together you can explore options to get your depression symptoms under control.

By Mayo Clinic Staff
Nov 27, 2007
© 1998-2007 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "," "EmbodyHealth," "Reliable tools for healthier lives," "Enhance your life," and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.

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