Foods you can eat when you have Multiple Sclerosis

Reverse MS Now

Heres just a few things youll learn about how to get back into health. and conquer Multiple Sclerosis. Those not-so innocent yet everyday substances that are currently attacking your body, perpetuating and aggravating your Multiple Sclerosis. What to do and what Not to do to overcome your Multiple Sclerosis effectively and permanently. How to create the energy you need to be able to work full time and feel confident you will be able to take care of your loved ones. How the pharmaceutical and food industry are conspiring to poison you and make you sick (Hint: American medical system is now the leading cause of death in the US). Read more...

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Complexity And Heterogeneity In Multiple Sclerosis

Self-evidently, the clinical phenotype of multiple sclerosis is variable with respect both to clinical features present in any one affected individual and disease patterns among groups. Clearly, the suggestion that a patient with brainstem involvement has a different disease from the individual with spinal cord involvement is not necessarily logical these differences more probably reflect the random involvement of different sites by the same pathological process. Furthermore, there is no evidence that the patient with infrequent episodes and full recovery enjoying prolonged periods of disease inactivity necessarily has a different disease from one in whom events move quickly through the relapsing, persistent and progressive phases of the disease. That is not to say that these two extremes of clinical course are definitely expressions of the same pathological sequence more that such variations are only evidence for complexity which may or may not indicate heterogeneity. The clinical...

Why Does Myelin Regeneration Fail In Multiple Sclerosis

In different experimental models of focal demyelina-tion, it has been shown that the adult rodent CNS has endogenous potential for regenerating oligoden-drocytes and myelin. Attempts to regenerate myelin can also be recognized pathologically in brains of multiple sclerosis patients by the existence of shadow plaques, which are partially remyelinated lesions.21-23 However, as disease advances, there is subsequent failure of remyelination. Data from experimental models of demyelination and from human brain tissue suggest that several factors may play a role in limiting myelin regeneration in the adult brain and its subsequent failure. In experimental focal demyelination it has been shown that only a subpopulation of local progenitor cells react to injury and generate new oligodendrocytes and myelin.17 Although progenitor cells were demonstrable in acute and chronic multiple sclerosis (MS) lesions, they did not exhibit reactive increases in cell number as compared to normal white...

Interferon betalb the first longterm effective treatment of relapsingremitting and secondary progressive multiple

Key words Interferon Beta-, multiple sclerosis Abstract Beta-interferons like other type I interferons are produced in response to viral infections by various mammalian cells. These include macrophages, dendritic cells and fibroblasts. Type I interferons have non-specific antiviral and anti-proliferative effects, as well as a broad spectrum of immunomodulatory activities. On this basis, type I interferons are used successfully in the treatment of viral infections such as hepatitis C, papilloma and HIV-1 virus. They are also used (mostly in combination with other drugs) to treat some forms of cancer, including leukemia. Whilst these effects could be anticipated from the biological function of type I interferons, it came as a surprise to most when a group of neurologists presented convincing clinical and laboratory evidence of a relevant and important effect of interferon beta-lb in multiple sclerosis (MS). These effects were first noted with regard to its earlier relapsing-remitting...

Interferonp In The Treatment Of Multiple Sclerosis

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS), affecting TABLE 7.5. Multiple sclerosis disease presentation and the location of CNS lesions About 80 of MS patients have an episodic form of the disease called relapsing-remitting multiple sclerosis. An episode typically starts with sensory disturbances, limb weakness, and clumsiness symptoms evolve over several days, stabilize, and then often improve spontaneously or in response to corticosteroids. In the initial phase of the disease, relapses are generally followed by complete or nearly complete clinical recovery. However, persistent signs of CNS dysfunction may develop after a relapse, and the disease While the specific mechanisms of action of interferon a and interferon-b1b in MS are not fully understood, each interferon has a number of immune-mediating activities (see Section 7.1). A recent review article on multiple sclerosis observed The interferons reduce the...

Cognitive and affective disturbances in multiple sclerosis

Neuropsychological disturbances and psychiatric problems are common in multiple sclerosis (MS).2-7 It is difficult to differentiate which of the disturbances are due to organic disease and which are psychological reactions to a disease which is always an enormous psychological burden, with its unpredictable course and potential to lead to severe disability and handicap.

Multiple Sclerosis

There are two reasons to choose multiple sclerosis (MS) as a representative model on which to base generalizations about pain in neurologic disease. AIDP, acute inflammatory demyelinating polyneuropathy DM, diabetes mellitus DMD, Duchenne muscular dystrophy HMSN, hereditary motor and sensory neuropathy ICP, intracranial pressure MS, multiple sclerosis PD, Parkinson's disease. AIDP, acute inflammatory demyelinating polyneuropathy DM, diabetes mellitus DMD, Duchenne muscular dystrophy HMSN, hereditary motor and sensory neuropathy ICP, intracranial pressure MS, multiple sclerosis PD, Parkinson's disease. Pain in multiple sclerosis

Matrix metalloproteinases and their inhibitors in brain injury and repair

MMPs appear to play a key role in the patho-genesis of central nervous system (CNS) disorders, contributing to blood-brain barrier (BBB) eruption, brain edema, immune cell infiltration, myelin degradation and glial-scar formation. Increased activity of MMPs has recently been reported in experimental animal models of demyelinating diseases as well as in multiple sclerosis (MS) patients. Similarly, increased levels of MMPs, and in particular MMP-2 and -9, have been detected in experimental cerebral ischemia as well as in stroke patients. Modulation of MMP TIMP profiles seems to be associated also with bacterial and viral meningoencephalitis. Additionally, though results are still controversial, MMPs seem to be involved in the deposition of p-amyloid protein in Alzheimer's diseases (AD).

Human Tcell lymphotropic virus type

Human T-cell lymphotropic virus type 1 (HTLV-1) infection is seen predominantly in the equatorial regions of southeastern Japan, the Caribbean, Africa, and Central and South America. Its routes of transmission are thought to be sexual, perinatal and by contact with contaminated blood.178 Most infected individuals remain asymptomatic. Affected patients present with back pain or painless progressive spastic paraparesis with constipation and urinary urgency or incontinence.179 HTLV-1 myelopathy (HAM), also know as tropical spastic paraparesis (TSP), has a highly variable disease course. Symptoms often stabilize within a few years of onset. Serum ELISA for HTLV-1 may establish the presence of the virus. CSF demonstrates elevated intrathecal synthesis of anti-HTLV-1 IgG. MRI reveals atrophy of the thoracic spinal cord and white matter lesions that can mimic those seen in multiple sclerosis. Although the exact pathogenesis is not well understood, virus particles and virus-infected T- and...

Fatigue As A Symptom In

Logical disorders such as multiple sclerosis (MS) or Parkinson's disease.4 Fatigue symptoms in MS are very similar to CFS, and there is additional evidence to support a common pathophysiology of fatigue in both these disorders.56 In addition, both MS and CFS patients with fatigue have a significantly lower frequency of psychiatric diagnosis than the depressed controls.7

Primary Angiitis Of The

Histological verification is not only to confirm the vasculitis, but to exclude other diagnoses which may mimic vasculitic syndromes, such as multiple sclerosis or its variants, primary brain lymphoma, infectious encephalitis, amyloid angiopathy, vascu-lopathy due to hypertension and or athersclero-sis.8,15-17 Therefore, histological verification is necessary in patients who are evaluated for the differential diagnosis of vasculitis. In addition, tissue diagnosis is important in these patients before initiating long-term immunosuppressive treatment that is known to have significant complications. Although limited in number, it has been our experience to see patients who presented with relatively acute onset of multifocal neurological signs and symptoms, who had changes consistent with vasculitis on their MRIs and angiographies, and in whom brain biopsy disclosed non-specific ischaemic changes or was not diagnostic. After treating the acute episode, we withheld long-term...

Brain biopsy in PACNS

Histological confirmation is the gold standard for the diagnosis of PACNS. As mentioned before, brain biopsy is important not only to confirm the diagnosis, but also for the exclusion of a number of other conditions which may mimic vasculitis. Vasculo-pathy due to hypertension and atherosclerosis, multiple sclerosis or its variants, sarcoidosis, primary brain lymphoma and other lymphoprolifer-ative diseases, primary or metastatic brain tumours, and infectious encephalitis such as neurocysticerco-sis, cytomegalovirus, herpes simplex, fungal infections, progressive multifocal leukoencephalopathy and Creuzfeldt-Jacob disease were some of the diagnoses found in patients referred for a brain biopsy with a suspected clinical diagnosis of PACNS (Table 20.1).8,15,16

Premorbid Personality

Repeated attempts have been made, in retrospective investigations of patients already affected, to characterize a premorbid personality, and to determine characteristics of personality which dispose to the disease. Such investigations8 claimed that the premorbid personality of MS patients should be characterized by hysterical aspects, as notes on 'hysteria' are frequently found in case reports of MS patients. In fact, MS may manifest itself in earlier phases of the disease by various symptoms which may be found in hysterical ('histrionics') personalities sensory disturbances, emotional instability, and particularly fatigue. If, from such observations, the inference is made that hysterical characteristics of personality may dispose to the development of MS, it only discloses a lack of ability to diagnose early manifestations of MS. 'In its infancy multiple sclerosis used to be called hysteria' said the famous Queen Square physician Farquhard Buzzard more than 100 years ago. Usually the...

Neurophysiology of inflammatory demyelinating disease

Disease Hysteria

Diseases such as multiple sclerosis (MS) and Guillain-Barre syndrome (GBS) result in inflammatory demyelinating lesions within the central and peripheral nervous systems (CNS, PNS) respectively. The lesions cause a range of conduction abnormalities and these lead directly to the symptoms expressed. The nature of the particular symptoms expressed depends upon the pathway affected by the lesion.

Matrix Metalloproteinases In Cidp

MMPs are able to degrade subendothelial basement membranes and may therefore act as effector molecules of blood-nerve or blood-brain barrier disruption.77 MMPs are upregulated in infiltrating immune cells in acute multiple sclerosis (MS) plaques and brain tissue in experimental autoimmune encephalitis.78,79 Studies have shown that interferon beta (IFN-p) suppresses the production of MMPs in T-lymphocytes and thus downregulates transbasement membrane migration.80 Consequently, inhibition of MMP activity seems to be one mechanism by which IFN-p down-modulates inflammatory activity. In experimental allergic neuritis (EAN), a model of acute inflammatory demyelinating polyneuropathy, an upregulation of MMPs has been described during the initial phase of the disease, with peak levels coincident with maximum clinical disease activity.81 The potential consequences of elevated level of MMPs in EAN comprise blood-nerve barrier damage, leukocyte extravasation, enhancement of the release of the...

The Common Clinical Pattern

Paroxysmal manifestations in multiple sclerosis share several clinical characteristics. They correspond to positive symptoms or signs related to hyperactivity of the central nervous system. They occur suddenly, at any time or place. Their duration is short, a few seconds to 1 or 2 min. They often recur from a few times per day to several times an hour. Their semiological expression may vary considerably from one patient to another, but, as shown on the occasion of the frequent recurrences, remains stereotyped for a given patient. Paroxysmal manifestations may either occur spontaneously or be triggered by external stimuli. Typical examples are neck flexion for Lhermitte sign, tactile stimuli for trigeminal neuralgia, and limb movements for kinesigenic choreoathetosis. Eye movements have also been described at the origin of phosphenes in Figure 30.1 Comparison of the clinical characteristics of paroxysmal manifestations, epileptic seizures, Uhthoff phenomenon and exacerbations in...


Promotion of CNS remyelination remains an important goal for the treatment of multiple sclerosis. Our laboratory has proposed the use of immunoglobu-lins directed at CNS antigens as an approach to enhance myelin repair. We have identified a panel of monoclonal antibodies which promote remyelina-tion in a virus-induced model of demyelination in mice. These antibodies are primarily of the IgM isotype and react to surface antigens on oligoden-drocytes. We are testing two major hypotheses to explain the mechanism of antibody-mediated myelin repair. The direct hypothesis proposes that antibodies react to surface antigens on oligodendrocytes to induce differentiation and or proliferation of these cells. The indirect hypothesis proposes that antibodies bind to injured myelin and or oligodendrocytes, resulting in more efficient scavenging by macrophages, thus allowing endogenous repair to take place. Alternatively, the antibodies may function as immunomodulatory agents and enhance...

The Diagnosis

The main risk is of underestimating these manifestations. They are indeed transient, and often have an original, if not odd, expression also, many patients are reluctant to report them spontaneously, as they are afraid to describe disorders that could seem too extraordinary to be true. The clinician himself may be tempted to consider these manifestations as the expression of fatigue, which is often present in multiple sclerosis. He may find it difficult to individualize these paroxysmal manifestations when they develop within a chronic neurological deficit syndrome. The diagnosis itself may be discussed with regard to three main syndromes. This is notably the case when the paroxysmal manifestations correspond to the onset of multiple sclerosis. This may also be the case in overt multiple sclerosis, as an intercurrent disease may always appear. A first alternative diagnosis is migrainous aura. The aura is visual in most cases, which is exceptional in multiple sclerosis-related...


We are indebted to the Uppsala Group68 for the current interpretation of the pathogenesis of the paroxysmal manifestations of multiple sclerosis. This interpretation is based on several lines of evidence. The common clinical pattern described above is one of these. It is very close to that of epilepsy. The second line of evidence is the common pathology, the plaques of multiple sclerosis being characterized by the original combination of demyelination and axonal preservation. As multiple sclerosis primarily affects myelin, focal lesions are subcortical or located within the central white matter. The common mechanism of these paroxysmal manifestations is, similarly to epileptic attacks, paroxysmal hyperactivity of a group of neurons but, in contrast to epilepsy, from a subcortical or deep area, i.e. axonal and not neuronal. This is the basis for the theory of ephaptic transmission. Considering the plaque of demyelination with axonal preservation, transmission of the nerve influx in one...


The paroxysmal manifestations in multiple sclerosis are among the most satisfactory symptoms to treat in multiple sclerosis. The treatment must first of all be symptomatic. It is based on the antiepileptic drugs, among which carbamazepine holds the first place. Its outstanding efficiency was first reported by Espir and Walker.16 Low doses may be effective. In some cases, one must resort to higher doses like

Box 34 Antibodies And Derivatives Used As Biotherapeutic Agents And Their Specific Targets

Interferon Beta Use in Multiple Sclerosis The first interferon beta for treatment of multiple sclerosis (MS) Betaseron (interferon beta-1b) received FDA approval in July 1993, based on a placebo-controlled study evaluating the incidence of exacerbations. Subsequently, a second interferon beta, Avonex (an interferon beta-1a), was shown to be effective for reducing the incidence of exacerbations and reducing the accumulation of physical disability. Betaseron received orphan drug designation prior to approval, and was still within the seven-year period of marketing exclusivity at the time Avonex was under review. However, Biogen, the manufacturer of Avonex, provided evidence that Avonex was not the same drug as Betaseron within the meaning of the orphan drug regulations, by showing a significantly better safety profile with regard to skin necrosis at injection sites. Consequently, Avonex and Betaseron were deemed to be different drugs and Biogen received marketing approval for Avonex in...

Question And Answer Session

PARTICIPANT Just to add to the controversy about the translational aspects, maybe some MS experts can make some distinction that's better. There's a lot of controversy in multiple sclerosis regarding axonal pathology. So it is not clear that there is a lack of axonal neuropathy in these MS neurons.

Skeletal Muscle Relaxants

Baclofen, tizanidine, and dantrolene were effective compared to placebo in patients with spasticity (primarily multiple sclerosis). There was fair evidence that baclofen and tizanidine were roughly equivalent for efficacy in patients with spasticity, but insufficient evidence to determine the efficacy of dantrolene compared to baclofen or tizanidine. There was fair evidence that although the overall rate of adverse effects between tizanidine and baclofen was similar, tizanidine was associated with more dry mouth and baclofen with more weakness (Chou et al. 2004).

Choosing the Experimental Animal

Since NSC therapy has yet to be approved for human clinical trials, experimental animals must be used. Mice are generally used for several reasons. First, as mammals, they share many homologous features with humans which will be very important in years to come when these studies are translated into clinical trials. Since the murine genome has already been sequenced, one can easily correlate the murine genes and their human homologs. Additionally, we now have engineered many murine lines expressing specific models of human disease or CNS insult such as lesions, tumors, parkinsonism and global demyelination (as observed in multiple sclerosis and many congenital metabolic disorders). Logistically, mice are small, inexpensive and easily maintained. They have quick gestations and high pregnancy rates resulting in higher and more quicker yields than in other animal models. Lastly, mice can be exploited in a manner often considered unethical in humans and more highly developed animals.

Microarray Technology

For DNA microarrays, DNA sequences, DNA inserts of a library from PCR amplifications, cDNA clones, or synthetic oligonucleotides can be immobilized on an impermeable rigid support (e.g., glass) in matrix spots. These microarrays can be hybridized to labeled cDNA probes prepared from the mRNA extracted from the cell and tissue of interest. The hybridization of the probe to each array component is measured to provide a quantitative measure of the abundance of each array component in the probe. Currently, oligonucleotide-based DNA chips are generated by the in situ synthesis of short (20- to 30-nucleotide) DNA fragments by either photolithography on a chip (developed by Affymetrix, Santa Clara, CA) or ink-jet technology (developed by Rosetta Inpharmatics, Kirkland, WA). The latter offers more speed in producing an array and increases the number of elements that can be arrayed on a single chip. Hybridization to short oligonucleotides on a chip has a lower threshold of specificity than the...

Naa As A Marker For Neuronal Health

Are decreased include Alzheimer's disease, epilepsy, schizophrenia, multiple sclerosis and AIDS dementia complex (Table 1). Earlier, the decreases in NAA were interpreted to represent irreversible loss of neurons. However, more recent evidence indicates that these decreases also could represent reversible neuronal mitochondrial dysfunction. 53 Multiple sclerosis 45

Mitoxantrone And Related Quinones

Mitoxantrone is active in breast cancer, acute promyelocitic or myelogenous leukemias, and androgen-independent prostate cancer. Although early reports seemed to indicate that its cardiotoxicity was lower than that of the anthracy-clines,56 this claim has been subsequently challenged.57 Mitoxantrone has been recently approved for treatment of secondary progressive multiple sclerosis (MS).58 The rationale for this application stems from the fact that MS is considered to be an autoimmune disease where a heightened immune action results in the destruction of the myelin of the central nervous system, causing nerve impulses to be slowed or halted and leading to the symptoms of MS. Since chemotherapeutic

In Vivo Magnetic Resonance Spectroscopy

MRS quantitatively measures metabolites in the tissues of interest. It is capable of both characterizing the metabolites and quantitatively measuring the tissue concentration of each metabolite associated in the pathological-biochemical processes (82-85). The changes in metabolite concentration measured by MRS can be used as a pharmacodynamic biomarker for noninvasive evaluation of therapeutic response. The feasibility of MRS for evaluating therapeutic response has been shown in both preclinical and clinical studies. For example, choline and phosphocholine have an elevated concentration in tumor tissues as shown by 1H and 31P MRS. Quantitative measurement of choline and phosphocholine with MRS can be used as a biomarker for evaluation of the efficacy of choline kinase inhibitors in anticancer treatment. Figure 7 shows the in vivo 1H and 31P magnetic resonance spectra of HT29 human colon tumor xenografts in mice before and after the treatment with a choline kinase inhibitor, MN58b...

Pains Of Primary Neurogenic Origin Paroxysmal

Trigeminal neuralgia occurs in multiple sclerosis approximately 300 times more often than in the general population. It is generally similar in its presentation to the idiopathic condition, but tends to occur at a younger age and is more likely to be bilateral (which is extremely rare in the idiopathic disorder). It is generally responsive to treatment along similar lines to idiopathic tic doulour-eux,13 although microvascular decompression (in a small series) appeared less effective,14 and there also appears to be relative refractoriness to neurolytic surgical proce-dures.15 A 1994 study7 suggests a prevalence in the order of

General considerations

Effective treatment of pain in neurologic disease is seldom, if ever, disease specific. Burning central neuropathic pain is probably as likely to respond to a tricyclic antidepressant whether the disorder responsible is syringomyelia, multiple sclerosis, or spinal cord injury. Conversely, an antiepileptic drug that successfully treats trigeminal neuralgia in a patient with MS may be completely ineffective for lumbar back pain in the same patient. Rational management of pain in any patient with neurologic disease must start with an attempt to identify the nature of the likely pathophysiology giving rise to the pain (or pains).

Sea Anemone Toxins Interacting with Kv1 Channels

All these toxin-channel interaction studies have assisted in the design of new types of toxins, such as ShK-Dap22 a mutant peptide where K22 has been replaced by a diaminopropionic acid. Binding and electrophysiological studies have shown that ShK-Dap22 is a highly potent and selective blocker of the Kv1.3 channel with a 100-fold decreased affinity for Kv1.1, Kv1.4 and Kv1.6 channels (Kalman et al. 1998). NMR studies have shown that the overall structures of ShK and ShK-Dap22 are quite similar, but there are differences in the side chains involved in Kv1.3 binding (Kalman et al. 1998 Norton et al. 2004). A high expression level of Kv1.3 is considered as a marker for activated effector memory T cells (TEM cells), which are involved in the pathogenesis of autoimmune diseases. Therefore, the selective suppression of autoreactive TEM cells with Kv1.3 blockers might constitute a novel approach for the treatment of multiple sclerosis (MS) and other autoimmune diseases such as type-1...

Key Learning Points

Pain is common with multiple sclerosis (40-70 percent any pain type 30 percent central neuropathic pain). Central poststroke pain is most common after lateral medullary and thalamic infarctions and occurs in 2-8 percent of those with strokes in other locations. The literature most strongly supports the following medications for the treatment of at least one central neuropathic pain subtype gabapentin, pregabalin, lamotrigine, amitriptyline, and cannabinoids.

Naa Is A Surrogate Marker Of Neuronal Health

NAA as measured by MRS, is currently the best and most specific noninvasive marker of axonal pathology in multiple sclerosis. An issue has been raised, however, that NAA is expressed also by oligodendroglial lineage cells34-36. In order to investigate NAA specificity for white matter axons, transected and contralateral non-transected mature and developing rat optic nerves were analyzed by HPLC and immunohistochemistry37. In adult transected optic nerves, axons degenerated rapidly reflected by decreasing NAA levels (Figure 5A) while myelin profiles, oligodendrocytes and NG2+ oligodendrocyte progenitor cells (OPCs) remained abundant. Because NAA became undetectable in these axon-free nerves, the data suggest that neither differentiated oligodendrocytes nor adult OPCs contribute to detectable NAA levels in mature CNS white matter tracts in vivo37. 3.3 Dynamics of NAA in Multiple Sclerosis

Painful Mononeuropathies

Trigeminal neuralgia (TN), also known as tic douloureux, is a neuropathic pain condition affecting the facial area. The IASP defines TN as a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. Although etiologically it is most frequently associated with vascular compression of the trigeminal nerve, other causes are also observed between 2 and 4 of cases are associated with multiple sclerosis (MS) and tumors as the underlying cause account for approximately 2 ofcases.

Discovery Of New Medicines

Once the target disease has been selected then a mechanism to attack the disease process is chosen. As scientific advances increase the understanding of the pathophysiology of a disease then new routes to attack the disease become apparent. For example as it was discovered that asthma was primarily caused by inflammation, then the search for new anti-asthma compounds shifted from p receptor agonists to anti-inflammatory agents such as leukotriene antagonists. It is through better understanding of conditions such as Alzheimer's disease or Multiple Sclerosis that possible pharmacological approaches to treatment will arise.

Observation Of Drug Effect Using

Decreased NAA has often been interpreted as indicating decreased relative neuronal density either due to loss of neurons or atrophy of their processes. However' it has become clear that a low NAA can also be the consequence of neuronal metabolic dysfunction i.e.' neurons whose NAA concentration has decreased. In cell culture40 and rodent experiments41-43 NAA density decreased in response to a metabolic stress and then increased after removal of the stress. This recovery of NAA has been observed in humans in the resolving inflammatory lesions of multiple sclerosis and resolving strokelike lesions of patients with mitochondrial encephalomyopathies.44 Increases in NAA have also been demonstrated in response to therapeutic interventions' including interferon treatment of multiple sclerosis'45 cerebral revascularization for carotid stenosis'46 surgery for temporal lobe epilepsy'47 and zidovudine treatment of AIDS.48 We speculate that these increases in NAA could involve two mechanisms...

Clinical Relevance of LThreonine

L-Threonine has also been used as a possible therapy for amyotrophic lateral sclerosis (ALS). A systematic review of the data available on this subject revealed no evidence that l-threonine therapy influences beneficially the natural course of this severe disorder (Parton et al., 2003). A similar systematic review failed to reveal clear effects of l-threonine in the treatment of multiple sclerosis.

Neuropathic Pain Syndromes Associated with the Trigeminal Nerve Trigeminal Neuralgia

The patient presents with sudden severe lancinating facial pain usually on one side, often triggered by chewing, talking, or touch. The patient is pain free between attacks, which can range from seconds to minutes. Patients may be pain free for months or years but each period of painful attacks may last weeks or months. V2 and V3 and rarely V1 of the trigeminal nerve are affected. MRI may demonstrate compression of the trigeminal tract or root by blood vessel or tumor. The average age of onset is 50 years. If trigeminal neuralgia presents in a young patient, multiple sclerosis should be ruled out.

Significance Of Glutamate Transporter Function

Increases in the level of extracellular glutamate could lead to an increase in expression of glutamate transporters, and also an increase in functional uptake. Indeed, GLAST and GLT1 expression is elevated in the optic nerve during multiple sclerosis, and glutamate uptake in this disease has been shown to be increased (64). The increase in expression

Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive devastating neurological syndrome that produces upper and lower motoneuron loss, manifested as progressive limb and facial motor weakness, atrophy, spasticity and hyperactive reflexes, and eventually respiratory compromise and death. The disorder has currently an incidence of 1-2 per 10,000, which is comparable to that of multiple sclerosis. However, recent epidemiological evidence indicates that the incidence of ALS is increasing in many countries, suggesting a role for environmental factors in the cause of the disease. The disease is present worldwide, but with an increased incidence in regions of the western Pacific, among the Chamorros of Guam, the Auyu and Jakei of West New Guinea, and the Japanese in the Kii peninsula (1).

Pharmacology and pharmaceutics

Clinical pharmacology Relapsing-re-mitting MS is characterized by recurrent attacks of neurologic dysfunction followed by complete or incomplete recovery. The mechanisms by which Betaseron exerts its actions in multiple sclerosis (MS) are not clearly understood. However, it is known that the biologic response-modifying properties of interferon beta-1b are mediated through its interactions with specific cell receptors found on the surface of human cells. The binding of interferon beta-1b to these receptors induces the expression of a number of interferon-induced gene products that are believed to be the mediators of the biological actions of interferon beta-1b. F. Role in therapy Betaseron is useful for reducing symptomatic exacerbation in multiple sclerosis (MS) patients with relapsing-remitting disease. The drug should be considered in patients with clinically definite or laboratory-supported definite disease. It is not indicated in those patients with primary progressive MS....

Mechanism Of Action

Therapeutic uses Glucocorticoids commonly are combined with other immunosuppressive agents to prevent and treat transplant rejection. High dose pulses of intravenous methyl-prednisolone sodium succinate (solu-medrol, a-methapred) are used to reverse acute transplant rejection and acute exacerbations of selected autoimmune disorders. Glucocorticoids also are efficacious for treatment of graft-versus-host disease in bone marrow transplantation. Glucocorticoids are used routinely to treat autoimmune disorders (see Chapter 59) and acute exacerbations of multiple sclerosis (see below). In addition, glucocorticoids limit allergic reactions that occur with other immunosuppressive agents and are used in transplant recipients to block first-dose cytokine storm caused by treatment with muromonad-CD3 and to a lesser extent thymoglobulin (see below).

Overview of Gap Junctions

Form intercellular links between astrocytes,60-62 neurons,59-62-63 astrocytes-oligodendrocytes,64-66 astrocytes-neurons,67-70 and more recently microglia.71-73 Inflammation is a hallmark of various CNS diseases such as bacterial and viral infections, multiple sclerosis (MS), Alzheimer's disease, and cerebral ischemia. Changes in gap junction intercellular communication as reflected by alterations in Cx isoform expression have been associated with several of these CNS inflammatory diseases, including experimental autoimmune encephalomyelitis (EAE), an animal model for MS, Alzheimer's disease, and cerebral ischemia,74-79 which may have dramatic implications for the survival of neuronal and glial populations in the context of neuroinflammation.

Clinical pharmacology Interferons are

Pharmacokinetics The pharmacoki-netics of interferon beta-1a (Rebif) in patients with multiple sclerosis have not been evaluated. In healthy subjects, a single injection resulted in a peak serum concentration at about 16 hours after administration. The mean serum elimination half-life was 69 hours but varied widely. Following every-other-day subcutaneous injections, an increase in the area under the serum concentration versus time curve (AUC) of approximately 240 was observed. Clearance has been estimated at 33 to 55 liters h. E. Therapeutic response Two studies evaluated the safety and efficacy of Rebif in patients with relapsing-remitting multiple sclerosis. Study 1 was a placebo-controlled, 2-year trial in 560 patients with multiple sclerosis for at least 1 year. The primary efficacy end point was the number of clinical exacerbations. The mean numbers of exacerbations per patient over 2 years was 1.82 and 1.73 in those who received Rebif either 22 mg or 44 mg three times per week...

Astrid E Cardona and Richard M Ransohoff

Actions of chemokines and the interaction with specific receptors within the central nervous system (CNS) surpass their original defined role of leukocyte recruitment to inflamed tissues. Chemokine receptor expression by resident CNS cells is crucial for normal brain development and architectural organization, neuronal protection during inflammatory and neurotoxic challenges, and, among many others, protective mechanisms during inflammatory conditions such as multiple sclerosis. The chemo-kine chemokine receptor systems involved in such significant functions include CXCR4 CXCL12, CXCR2 CXCL1, and CX3CR1 CX3CL1. In this chapter, we discuss how these receptors might contribute to modulate communication within the CNS and with peripheral elements, and we also suggest potential mechanisms of action of fractalkine and the translation of these into the understanding of microglial function during neuro-inflammatory conditions. Key Words Chemokine receptors CNS multiple sclerosis microglia NK...

Expression of Chemokine Receptors in Cells Intrinsic to the Central Nervous System

Increasing evidence highlights the prominence of chemokines in a variety of physiologic and pathologic processes in the CNS. In particular, chemokines have been shown to be critical determinants in the positioning of cellular population in the development of CNS inflammation due to autoimmune reactions or infectious diseases (2,15). Several lines of evidence indicate that all resident cells of the CNS express functional chemokine receptors in the intact human brain and in the CNS of rodent and macaques as experimental models. Astrocytes and microglia express most of the chemokine receptors including CCR3 (16-18), CCR5 (17), CXCR3 (19-21), and CXCR4 (18,22,23). Functional expression of CCR2 by fetal human astrocytes (24) and by reactive microglia in multiple sclerosis (MS) lesions (25) has been documented. Confined exclusively to microglia in vivo is the expression of CX3CR1 (26,27). Neurons exhibit expression of CCR1 (28), CXCR1 (29), CXCR2 (29), and CXCR4. Neuronal CCR1 expression,...

Mechanism and Disease Associated PD Markers

PD markers related to the manifestation of disease include those that identify patient subsets prior to therapeutic intervention and those that change in response to treatment and may be useful for defining biological response in patient subsets. Multiple sclerosis (MS) is a disease in which the Pgx (both types) markers have been studied.

Brain drug delivery strategies via colloid carriers

Experimental autoimmune encephalitis is another brain disease in which PEGylated liposomes have been found useful for drug delivery. In inflammatory conditions, it is believed that the disruption of BBB allows the free diffusion of colloids such as liposomes. Thus, prednisolone entrapped into PEGylated liposomes has demonstrated an effective restoration of the BBB integrity macrophage infiltration was diminished in the treated animals. Additionally, the use of liposomes may reduce systemic side effects and could be employed for the treatment of multiple sclerosis (Schmidt et al., 2003).

Sea Anemone Pore Forming Toxins Actinoporins

Sea anemones are providing an ever-increasing array of toxins besides modifiers of Na+ and K+ channels, that have found some utility in the treatment of multiple sclerosis (Lewis and Garcia 2003 Norton et al. 2004) including cytolytic pore-forming toxins (Fig. 2). The most commonly described toxins are equinatoxin from Actinia equina and sticholysins from Stichodactyla helianthus, homologous 20 kDa polypeptides known to produce cation-permeant pores in sphingomyelin-containing membranes.

Limited access to the CNS

Clonidine Metabolites

Apraclonidine (Iopidine) and Brimonidine (Alphagan). In addition to its therapeutic use as an antihyperten-sive agent, clonidine has been found to provide beneficial effects in several other situations,47 including glaucoma, spasticity, migraine prophylaxis, opiate withdrawal syndrome, and anesthesia. This has prompted the development of analogs of clonidine for specific use in some of the mentioned areas. Two of such examples are apraclonidine and brimonidine. Apraclonidine does not cross the BBB. However, brimonidine can cross the BBB and hence can produce hypotension and sedation, although these CNS effects are slight compared with those of clonidine. CNS effects of these drugs are correlated well to their log P, pKa, and thus log D value. Both apraclonidine and brimonidine are selective a2-agonists with a1 a2 ratios of 30 1 and 1,000 1, respectively. Brimonidine is a much more selective a2-agonist than clonidine or apraclonidine and is a firstline agent for treating glaucoma....

Animal Models of Human Disease States

An analysis of 76 peer reviewed animal studies (Hackam & Redelmeier, 2006) in a variety of therapeutic areas including obesity, cancer, irritable bowel disorder (IBD), stroke, diabetes, experimental autoimmune encephalomyelitis (EAE), multiple sclerosis (MS), hypertension, and sepsis led to the conclusion that only about one-third (33 ) of highly cited animal research translated at the level of human randomized trials. Of the 76 studies, 34 (45 ) were untested, for example, failed to reach Phase III (D.G. Hackam, personal communication), 28 (27 ) were replicated, and 14 (18 ) contraindicated. For those compounds whose effects were replicated, 8 were finally approved for human use. To place the studies analyzed in context, replication rates in human studies were slightly higher (44 Ioannidis, 2005a) extending the question of rigor to the full spectrum of the biomedical research endeavor (Ioannidis, 2005b). Outcomes from the translational process have been further confounded by the...

Behavioral Effects Of Infectious Diseases And Cytokine Administration In Animals

Reduced Consumption of and Preference for Sweet Solutions. The consumption of and preference for sweet solutions can serve as a model for hedonic processes, because when presented with such solutions, animals will drink more fluid than they usually drink, and if given a choice, they will prefer these solutions over water. Moreover, non-hungry or thirsty animals will perform operant tasks to obtain sweet solutions as a rewarding stimulus, in the same way that they perform for ICSS and other rewards. Our studies demonstrated that various immune challenges attenuated the consumption of and preference for sweet solutions, while having minimal effects on water drinking (Table 1). LPS significantly decreased saccharin preference in fluid-deprived rats, and suppressed free consumption of saccharin solution in non-deprived rats water consumption was not affected under these circumstances (Yirmiya, 1996). A similar decrease in saccharin-, but not water-consumption was demonstrated...

Effects Of Antidepressants On Depression Induced By Immune Activation

Bendsen Signs

Antidepressants have been used successfully in treating depressive symptoms associated with various medical conditions (Katon & Sullivan, 1990). Both tricyclic antidepressants (TCAs) (Schiffer & Wineman, 1990) and selective serotonin reuptake inhibitors (SSRIs) (Scott, Nussbaum, McConnell, & Brill, 1995) have been used successfully in the treatment of depression associated with multiple sclerosis, stroke (Lauritzen, Bjerg Bendsen, Vilmar, Bjerg Bendsen, Lunde, & Bech, 1994), Alzheimer's disease (Gottfries, 1997 Tueth, 1995), HIV infection (Ayuso, 1994 Rabkin, Wagner, & Rabkin, 1994), and depression induced by IFN administration (e.g., in hepatitis C or multiple sclerosis patients) (Levenson & Fallon, 1993 Mohr, Goodkin, Likosky, Gatto, Baumann, & Rudick, 1997).

Mitochondrial Dna Variants And Aging

Mitochondrial ATP production via oxidative phosphorylation is essential for normal function and maintenance of human organ systems, and numerous mutations of mtDNA are known to cause severe maternally transmitted diseases. A common feature in this group of inborn diseases is the involvement of some enzymes in the pathway of aerobic energy production. Thus, these syndromes are characterized by defects in organs and functions where energy supply is of more importance such as muscles, heart, eye, and the central nervous system. Besides these pathogenic mutations, other maternally inherited variants of mtDNA are present in the population. The study of such variants of mtDNA led to the identification of several mtDNA haplogroups (groups of haplotypes derived from the same mtDNA ancestor). Those present in Europe are called H, I, J, K, T, U1, U2, U3, U4, U5, U6, v, W, X, and others. It is now emerging that such variants have to be considered as ''natural'' but not necessary ''neutral'' from...

Consequences Of Antibodies To Therapeutic Proteins

In the case of interferon beta treatment of multiple sclerosis the loss of efficacy is much more difficult to measure because the mode of action of the therapeutic protein is not known and the disease progress is unpredictable and difficult to monitor. The reduction of Mx induction which is specific for interferon activity has been used successfully to evaluate the biological effect of antibodies to interferon beta. The adverse effects of therapeutic proteins are in general the result of an exaggerated pharmacodynamic effect. So the loss of side effects may also be the result of the induction of antibodies and may be the first sign of immunogenicity. For example, in patients treated with interferon the loss of flulike symptoms is associated with the appearance of antibodies. Because by definition neutralizing antibodies interact with ligand-receptor interaction, they will inhibit the efficacy of all products in the same class with serious consequences for patients if there is no...

Role of Pharmacotherapy

This also means the adjustment disorders are difficult to study to ascertain their actual frequency in various populations. For similar reasons, it is difficult to study cohorts receiving various interventions in randomized controlled trials it is uncertain whether one has comparable patient groups when attempts are made to observe outcomes. Adjustment disorders have been diagnosed in over 60 of burn patients, greater than 20 of patients with multiple sclerosis, and over 40 of poststroke

Antisense Oligonucleotides

Paper Dna Printable Pattern

Of the ON is sufficient to activate RNase H.8 Interestingly, replacement of the phosphodiester bond by phosphorothioates throughout the gapmer allows further gain in nuclease stability without increasing the toxicity of the ON - a phenomenon that is not yet fully understood. Gapmer ONs that consist of MOE and phosphorothioate DNA monomers are currently in clinical development against a broad range of diseases, including diabetes, high cholesterol level, multiple sclerosis, psoriasis and cancer (Table 1.1). Multiple sclerosis

Other chimeric neurotoxins and novel approaches

To study the localization and function of neuronal targets of neuropeptide hormones, a variety of chimeric toxins of ricin A chain with oxytocin, atrial natriuretic peptide or gelonin with corticotrophin releasing factor have been prepared and characterized (Schwartz and Vale, 1989 Samson et al., 1992 1993 1995 Blackburn et al., 1995). Myelin basic protein (MBP) is an important component of myelinated neurons. Antibodies against MBP are generated in autoimmune diseases of the nervous system such as multiple sclerosis. Very promisingly, a chimeric toxin combining MBP and Pseudomonas exotoxin (MBP-PE40) blocked the clinical symptoms of inflammation and demyelination typical of this disease, providing a new immunotherapeutic tool (Brenner et al., 1999) for autoimmune nervous system diseases in which a known antigen is involved. The poor prognosis associated with

Traumatic Brain Injury

Canavan Disease

Reduced NAA concentrations can reflect neuronal death, but this mechanism cannot account for the reversible decreases in NAA observed in multiple sclerosis 22 and stroke 23 , or the possible increases over time, post-injury, observed in our TBI sample 18 . Given Gasparovic's results, and the fact that our NAA analyses were undertaken in normal appearing tissue, it may well be the case that individual variation in metabolism, rather than loss of neurons, underlies the well-established relationship between NAA and concurrent and long term cognitive function. Consistent with this possibility, Positron Emission Tomography analysis has shown that NAA concentrations correlate with overall metabolic rate 24 , which is often reduced after TBI.

Stem Cell Transplantation Methods

J fust a few short years ago, we still used to think that we were born with a finite number of I irreplaceable neurons. However, in recent years, there has been increasingly persuasive evidence I that suggests that neural stem cell (NSC) maintenance and differentiation continue to take ace throughout the mammal's lifetime. Studies suggest that neural stem cells not only persist to mammalian adulthood, but also play a continuous role in brain tissue repair throughout the organism's lifespan. These preliminary results further imply that NSC transplantation strategies might have therapeutic promise in treating neurodegenerative diseases often characterized by isolated or global neuronal and glial loss. The destruction ofneural circuitry in neuropathologies such as stroke, Parkinson's disease, MS, SCI prevents signals from being sent throughout the body effectively and is devastating and necessitates a cure.NSC transplantation is among one of the foremost researched fields because it...

About the Editor

Konat is a professor in the Department of Neurobiology and Anatomy, West Virginia University School of Medicine, Morgantown. He obtained his research training in biochemistry with a master's degree from the University of Warsaw and a doctorate from the University of Southern Denmark. Prior to joining the West Virginia University faculty, he worked at several institutions, namely, the Medical Research Center of the Polish Academy of Sciences in Warsaw, the Neuro-chemical Institute in Copenhagen, the University of Copenhagen, the University of Texas Medical School at Houston, and the Medical University of South Carolina in Charleston. Dr. Konat's initial research interests centered on central nervous system myelination and myelin disorders. In particular, his endeavors involved studies of the assembly of myelin membrane, the regulation of myelin gene expression, as well as the pathochemistry and immunology of multiple sclerosis. His current research emphasis has shifted...


Castaneda et al.23 at Genentech Inc. reported the solid-phase synthesis of a4Pj a4P7 integrin antagonists. Because it is believed that a4P7 plays a role in inflammatory bowel disease, while a4P1 plays a role in diseases such as asthma and multiple sclerosis, finding selective ligands for these integrins could serve as therapeutic agents to alleviate or control such diseases.


Tizanadine is marketed for the treatment of muscle spasm associated with multiple sclerosis but since it has an a-adrenoreceptor agonist effect one would expect it also to have analgesic properties. This supposition is backed up, to a certain extent, by study and case report evidence.

Movement Disorders

In common with multiple sclerosis, it seems likely that pain is underestimated in these conditions, although there are fewer data available from the medical literature to support this assertion. The likelihood of nociceptive pain in patients with impaired involuntary movement seems intuitively obvious, but there is evidence of neuropathic pain in some of these disorders as well, focusing attention on involvement of sensory, as well as motor tract pathology.


To summarize the findings, the majority of studies were of neuropathic pain states, with three examining diabetic neuropathy. Results were conflicting. Overall, NNT for both effectiveness and adverse effects were similar to the corresponding figures for the anti-depressants. The relatively new adjunctive anticonvulsant gabapentin was not included in this review, but a number of subsequent publications report benefit in pains associated with multiple sclerosis,43, 44, 45, 46 V diabetic neuropathy, PHN, and other neuropathic pain states. Pregabalin is also clearly effective,47 although good evidence of superiority over gabapentin is lacking. There is also growing evidence of benefit from lamotrigine in central pain.41 I , 48 V Adverse effects frequently limit the practical utility of antiepileptic drugs, with a recent study of patients with MS showing that carbamazepine was associated with worse adverse effects than either gabapentin or lamotrigine, in some cases mimicking disease...

Concluding Comments

Channels like ASICla and ASIC3 which are expressed in nociceptive neurons, have been implicated in inflammation and in various pain processes (Mazzuca et al. 2007). Voltage dependent K+ channels are key elements in the repolarization phase and duration of action potentials, consequently they are very important in a number of physiological processes. Dysfunctions of K+ channels often correspond to diseases such as episodic ataxia (Kvl.l), cardiovascular disorders (KCNQ1, HERG), neonatal convulsions (KCNQ2, KCNQ3) and deafness (KCNQ1, KCNQ4). It is very important to find molecules that are able to selectively interact with these channels. The most important sources of such molecules are animal venoms. SAK toxins which block some Kv channels, by their original mode of action and their particular structural properties, are important additions to the currently known panel of natural Kv inhibitors isolated from other animal venoms. SAK toxins target Kv1, HERG and Kv3 channels subfamilies,...


As one might expect, the prevalence of neuropathic pain is markedly higher among patients with diseases known to cause neuropathic pain, such as diabetes (40-50 ) (Veves et al. 2008), HIV infections (38-62 ) (Simpson et al. 2006, Cherry et al. 2006, Morgello et al. 2004), and multiple sclerosis (27.5 ) (Osterberg et al. 2005), as well as those with known or suspected neuronal injury such as trigeminal neuralgia, glossopharyngeal neuralgia, and postherpetic neuralgia. However, it is less well recognized that neuropathic pain has been reported after a range of different types of common surgical procedures such as tho-racotomy, inguinal hernia repair, and mastectomy. In one of the largest studies conducted to date investigating neuropathic pain following thoracic surgery, Maguire et al. found that at 1 year following video-assisted thorascopic surgery (VATS), 57 of patients experienced neuropathic pain symptoms that significantly interfered with their daily activities (Maguire et al....

Trigeminal Neuralgia

Trigeminal neuralgia (TN) is defined by the International Association for the Study of Pain (IASP) as a sudden, usually unilateral, brief stabbing recurrent pain in the distribution of one of more branches of the trigeminal nerve. TN is usually divided into classical or idiopathic TN and symptomatic or secondary TN. For classical trigeminal neuralgia (CTN), there is no apparent cause other than vascular compression (see under Pathophysiology), whereas for symptomatic trigeminal neuralgia (STN) there are structural lesions, for example multiple sclerosis or compression of the posterior fossa.102


As the first DNA recombinant technology products effective in cancer treatment, IFNs opened an era of biologic therapies for cancer, multiple sclerosis, and infectious diseases. Although more than 40 years have passed since IFNs were first described, scientific and clinical interest in these multifunctional cytokines has not diminished. The mechanisms of antitumor effects, optimal dose, schedule, and type of IFN for specific clinical indications have yet to be fully described. Progress in cloning IFN receptors and other signaling components has allowed further identification and description of molecular pathways by which IFNs mediate their effects. Further characterization and identification of in-terferon-stimulated genes or factors that mediate IFN-dependent antiproliferative, apoptotic, and immunomodulatory effects will lead to better utilization of IFNs in the treatment of cancer. Innovative approaches such as the introduction of second-generation IFNs with different biological...

Interferon Beta1a

Indications Treatment of relapsing-remitting forms of multiple sclerosis (MS) to slow the accumulation of physical dis B. Indications and use Avonex is indicated for the treatment of relapsing forms of multiple sclerosis to slow the accumulation of physical disability and decrease the frequency of clinical exacerbations. Safety and efficacy in patients with chronic progressive multiple sclerosis have not been evaluated.


Hellman et al. (27) studied the effects of IFN-P on the CYP2C19 and CYP2D6 activities in patients with multiple sclerosis. There were 10 Caucasian patients with multiple sclerosis who received IFN-P1a (AVONEX) 30 mg weekly intramuscularly, Rebif 22 or 44 mg thrice weekly SC, or IFN-P1b (Betaferon) 250 mg every other day SC. The urinary S R mephenytoin ratio (for determination of CYP2C19 activity) and debrisoquine metabolic ratios (for determination of CYP2D6 activity) were used to characterize the activity of the two CYPs. The results of the study indicated that one-month IFN-P treatment did not alter CYP2C19 or CYP2D6 activities.


Poor manganese status has been implicated in a variety of disease states and metabolic disorders, including osteoporosis, congenital malformations, TPN, Perthes' disease (necrosis of femur head), senile cataracts, epilepsy, amyo-trophic lateral sclerosis (degenerative disease of motor neurons), acromegaly (pituitary disorder of excess growth of extremities and face), hip abnormalities, multiple sclerosis,23 phenylketonuria (congenital defect causing mental retardation) and maple syrup urine disease (neurodegenerative disease of amino acids in urine).8 One exacerbating factor is the iron intake and status of an individual, as both iron and manganese share a common transport protein in the blood (transferrin) and cell (divalent metal transporter DMT1). In young women, a supplement of 60 mg Fe day for 4 months decreased activity of leukocyte manganese.24 Also, manganese absorption was lowered in women with high ferritin, the iron storage protein.25


Interferon beta-1a (avonex, rebif), a 166-amino acid recombinant glycoprotein, and interferon beta-1b (betaseron), a 165-amino acid recombinant protein, have antiviral and immunomodulatory properties. They are FDA-approved for the treatment of relapsing and relapsing-remitting multiple sclerosis to reduce the frequency of clinical exacerbations (see below). The mechanism of their action in multiple sclerosis is unclear. Flu-like symptoms (fever, chills, myalgia) and injection-site reactions are common adverse effects. The use of these and other interferons in the treatment of viral diseases is discussed in Chapter 49. A CASE STUDY IMMUNOTHERAPY FOR MULTIPLE SCLEROSIS clinical features and pathology Multiple sclerosis (MS) is a demyelinating inflammatory disease of the CNS white matter that displays a triad of pathogenic features mononu-clear cell infiltration, demyelination, and scarring (gliosis). The peripheral nervous system is spared. The disease, which may be episodic or...

Interferon Beta1b

Indications Treatment of ambulatory patients with relapsing-remitting multiple sclerosis to reduce the frequency of clinical exacerbations B. Indications and use Betaseron is indicated for use in ambulatory patients with relapsing-remitting multiple sclerosis to reduce the frequency of clinical exacerbations. The safety and efficacy of Betaseron in chronic-progressive MS has not been fully evaluated.

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