Natural Ways to Treat Multiple Sclerosis

Dr Garys MS Treatment System

The healing process is done by using a simple step-by-step method that rehabilitates your immune system and boosts supporting body systems to get rid of all symptoms (and types) of Multiple Sclerosis PLUS re-energizes and purifies your body for maximum health. In the step-by-step Treatment System, you'll learn how my Directed Nutrition method plus a special vitamin regimen will significantly reduce your symptoms and eventually completely rid you of your current condition. The beauty of ALL Natural treatments is that there are NO Side Effects. You won't see a side effect disclaimer associated with my MS treatment because it WILL NOT make anyone sick. All Natural means you save money on costly prescription drugs and you avoid harsh side effects, all while receiving improved benefits fighting MS. Read more...

Dr Garys MS Treatment System Summary

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Demyelinating diseases 1071 Multiple sclerosis

Multiple sclerosis (MS) was recognized by the mid 19th century, and already in 1871 Hammond referred to it as a cerebrospinal sclerosis it was Charcot who, in 1877, realized the role of disrupted myelin in the pathogenesis of this disease. MS is an inflammatory demyelinating disease of the CNS, which culminates in progressive neurological deterioration. The aetiology of MS remains elusive, as both genetic predisposition and environmental factors are indicated. The importance of genetic predisposition is evident from very high concordance of the disease occurrence between monozygotic twins, whereas the environmental factors are implicated by the existence of geographical areas with remarkable differences in MS prevalence (generally, MS is significantly more frequent in northern than in southern parts of the world). The general theory regards MS aetiology as an infection which presents the immune system with an antigen similar to CNS myelin the resulting antibodies eventually attack CNS...

CMC1R and Multiple Sclerosis

MC1R RHC variants R151C, R160W, and D294H have been associated with increased risk of multiple sclerosis (MS),407,408 while the D84E allele was associated with increased severity of MS.407 This association was unexpected, as increased UVexposure or vitamin D synthesis is associated with a decreased risk of MS. The hypothesized explanations for this discrepancy include that RHC variant allele carriers behave in a sun avoidant manner, or that the loss of MC1R-mediated anti-inflammatory effects (see above) in RHC allele carriers contributes to MS risk.408

Multiple sclerosis

Multiple Sclerosis (MS) is a chronic T-cell mediated demyelinating autoimmune disease of the central nervous system. Disease onset usually occurs between 20 and 40 years of age, after which progression is variable, but generally slow. The geographic distribution of the disease has led to much debate over the relative importance of racial susceptibility (presumably genetic) and environment. On the one hand, there is a strong gradient towards higher prevalence at higher latitudes, both north and south of the equator on the other, there are marked deviations from this pattern, including a high prevalence among Sardinians and Palestinians, and low prevalence among Chinese and Japanese, black Africans, Maoris and Amerindians (Rosati, 2001).

Routes of administration

For longer-term feeding, pharyngostomy and oesophagos-tomy are used by some surgeons. Surgically placed gastrostomies are used for long-term administration of feed for patients with progressive deglutition disorders (motor neurone disease, multiple sclerosis). Stamm gastrotomy (Fig. 4.2) is simple to perform as a temporary procedure. The removal of the tube is rapidly followed by closure of the cutaneous orifice. The percutaneous endoscopically-placed gastrostomy (PEG) is now the technique of choice for long-term administration of EN. This technique has a lower morbidity and mortality, when compared with the conventional surgical placement. A needle catheter jejunostomy is shown in

Susceptibility Linkage

It has long been recognized that, despite living at geographical latitudes where multiple sclerosis (MS) is common, genetically isolated ethnic groups including Gypsies in Hungary (1) Indians and Orientals in North America (2) Aborigines in Australia (3) and Maoris in New Zealand (4) remain resistant to the disease. Systematic analysis of familial aggregation of MS in particular, studies of twins (5-8), adoptees (9), and half-siblings (10) has also confirmed Eichhorst's description from the 1890s of MS as a heritable disorder (11). The degree to which a disease is heritable can be estimated by dividing the lifetime risk of siblings to affected individuals by the population prevalence of the disease, to yield the so-called ks statistic. For MS, in high-risk populations, ks is between 20 (0.02 0.001) and 40 (0.04 0.001) a value similar to that seen in insulin-dependent diabetes mellitus (12). Data from twin studies which show that the concordance rate of approximately 30 in monozygotic...

Biological aspects of variants A and B

HHV-6 infects a wide variety of cell types including diploid lung fibroblasts, neural cells, megakaryocytes and NK cells. In most of these cell lines there is a low level of viral replication. It has been shown that HHV-6A induces CD4+ receptor on CD8+ cells, making them infectable with HIV. It has also been shown that B-lymphocytes are not infectable with HHV-6A, but Epstein-Barr virus (EBV)-pos-itive B-lymphocytes can be infected with HHV-6A. It was reported that HHV-6A, not HHV-6B, activates EBV and similarly HHV-6A also activates HHV-8 (Flamand et al., 1993 Cuomo et al., 1995 Zeng et al., 2005). It was also shown that HHV-6A induces cell membrane receptor expression that predisposes them to superinfection by other viruses, such as EBV and HIV (Krueger et al., 1990 Schonnebeck et al., 1991). HHV-6B (Z-29) grew best in HTLV-1 transformed cell line MOLT-4, which is not infectable with HHV-6A. The propagation and replication of HHV-6A and B isolates have been studied. HHV-6A (GS...

Disease associations of HHV6A and 6B variants

It was previously thought that primary infection of HHV-6 in infants and young children lead to roseola and febrile illnesses. This infection was attributed to HHV-6B (Yamanishi et al., 1988). Some of the symptoms identified include diarrhea, vomiting, seizure, nasal congestion, rash and high fever. Similar symptoms were noted in Africa in children and the DNA analysis from the peripheral blood from these children revealed HHV-6A infections (Hidaka et al., 1997 Kasolo et al., 1997 Randhawa et al., 1997). It is, therefore, obvious that both variants A and B participate in infecting growing children with identical pathologies. Hall et al. (1994) also observed that one third of congenital infection was due to HHV-6A. Later on these children still retained HHV-6A DNA. There have not been longitudinal follow-up studies to assess whether these children with congenital HHV-6A infection could be at risk of developing a central nervous system (CNS) illness such as multiple sclerosis.

Serologic assays Techniques

A current trend is the identification of target proteins by means of immunoblot or immunoprecipitation assays combined with the use of monoclonal antibodies (Balachandran et al., 1989). Such approach has permitted to recognize the protein p100 (U11 gene product) as a major determinant of immune response (Yamamoto et al., 1990 Neipel et al., 1992). Similarly, a 101 kDa protein (101K) has been identified as an immunodominant virion protein for both IgG and IgM reactivity (LaCroix et al., 2000). The early antigen p41 38 (U27 gene product) had been chosen to develop a specific ELISA (Iyengar et al., 1991 Patnaik et al., 1995a). This early protein has been found to contain a divergent epitope which permits to differentiate HHV-6A from HHV-6B (Xu et al., 2001). However, further results obtained with recombinant p41 as the ELISA antigen have been rather disappointing both in terms of overall serum reactivity and variant specificity (Xu et al., 2002). The residues 4-10 of U24 gene product...

Lymphatic and hematopoietic system see also chapters 14 and

HHV-6 replicates with low efficiency in neuroglial cells (Luppi et al., 1995). Viral DNA and antigen have been successfully demonstrated in human brain tissue, both in healthy organs and in diseased tissues, with subtype A being about three times more frequent than subtype B (Fig. 2 Luppi et al., 1995 Hall et al., 1998 Cuomo et al., 2001). There are increasing reports of HHV-6-associated meningitis, encephalitis in children with febrile seizures (Caserta et al., 1994 Wilborn et al., 1994 Knox and Carrigan, 1995 Bonthius and Karacay, 2002 Eeg-Olofsson, 2003), acute necrotizing or hemorrhagic encephalitis and demyelinating brain diseases in immune-deficient patients and in persons suffering from multiple sclerosis (Challoner et al., 1995 Wagner et al., 1997 Solldan et al., 2000 An et al., 2002 Cirone et al., 2002 Chapenko et al., 2003 Tejada-Simon et al., 2003). CNS infections with HHV-6 appear more frequent in patients with T-cell immune deficiency (Pruitt, 2003).

The Chronic Inactive MS Lesion

Figure 1 (See color insert.) Chronic multiple sclerosis. Grossly, plaques appear as well-circumscribed, slightly depressed gray areas of increased tissue texture. The chronic inactive plaque microscopically appears as a sharply circumscribed area of myelin pallor (A, LFB PAS) with variable reduction in axonal density (B, neurofilament protein). The lesions are hypocel-lular and lack macrophages containing myelin debris (C, KiMlP for macrophages). Abbreviation LFB PAS, luxol fast blue periodic acid schif. Figure 1 (See color insert.) Chronic multiple sclerosis. Grossly, plaques appear as well-circumscribed, slightly depressed gray areas of increased tissue texture. The chronic inactive plaque microscopically appears as a sharply circumscribed area of myelin pallor (A, LFB PAS) with variable reduction in axonal density (B, neurofilament protein). The lesions are hypocel-lular and lack macrophages containing myelin debris (C, KiMlP for macrophages). Abbreviation LFB PAS, luxol fast blue...

What Is The Pathogenic Role Of Inflammation In Ms

Figure 5 (See color insert.) Inflammation in multiple sclerosis lesions. The inflammatory infiltrate within an active multiple sclerosis lesion contains variable numbers of perivascular and parenchymal CD3+ T-lymphocytes (A), cytotoxic CD8+ T-lymphocytes (B), macrophages (C KiMIP), CD20+ B-lymphocytes (D), and plasma cells (H&E). Figure 5 (See color insert.) Inflammation in multiple sclerosis lesions. The inflammatory infiltrate within an active multiple sclerosis lesion contains variable numbers of perivascular and parenchymal CD3+ T-lymphocytes (A), cytotoxic CD8+ T-lymphocytes (B), macrophages (C KiMIP), CD20+ B-lymphocytes (D), and plasma cells (H&E).

Positron Emission Tomography PET Imaging and Single Positron Emissions Computed Tomography Imaging

PET imaging may still prove useful in future HIV studies. There are many new and novel tracers developed over the past several years that have the potential to examine very specific metabolites and or neurotransmitters. For example, the use of the PET ligand 11C -PK11195 might provide a window into active areas of inflammatory processes in HIV infection. Examination of multiple sclerosis (MS) patients using this ligand has demonstrated increased sensitivity of MS activity, often extending into normal appearing white matter, especially during active clinical phases of the MS activity (Vowinckel, Banati, Debruyne). Thus, there may be additional opportunities to examine the effects of HIV-associated CNS injury using PET technology.

Oligodendrocyte Pathology and Early Remyelination

Figure 6 Electron microscopy of an early multiple sclerosis lesion reveals active demyelination occurring simultaneously with remyelination. A macrophage containing myelin debris is in proximity of both completely demyelinated axons (Ax), as well as thinly remyelinated axons (*). Source Photo courtesy of Dr. Moses Rodriguez, Mayo Clinic, Rochester, Minnesota, U.S.A. Figure 6 Electron microscopy of an early multiple sclerosis lesion reveals active demyelination occurring simultaneously with remyelination. A macrophage containing myelin debris is in proximity of both completely demyelinated axons (Ax), as well as thinly remyelinated axons (*). Source Photo courtesy of Dr. Moses Rodriguez, Mayo Clinic, Rochester, Minnesota, U.S.A.

Modulation of Lymphocyte Homing for Therapeutic Purposes

Recent events have prompted intense discussion on the validity of this argument. Clinical trials with Natalizumab (Tysabri), a mAb that blocks the binding of both a401 (VLA-4) to VCAM-1 and a407 to MAdCAM-1 on Th1 cells that infiltrate the brain and gut, respectively (von Andrian and Engelhardt 2003), have shown that the mAb is efficacious in the treatment of both Crohn disease (Ghosh et al. 2003) and, especially, multiple sclerosis (Miller et al. 2003). These exciting clinical results were initially hailed as validation

Summary and Future Research

Another significant improvement that will advance the HIV infection literature will be larger, prospective studies. To date, the vast majority of imaging studies are cross-sectional in design. There are a few notable exceptions, though these studies are often limited to smaller cohorts and limited time points (not more than two time points). One major advantage of prospective studies is the improved statistical power when using participants as their own controls. There has been much work recently reported in the literature, regarding time series analyses of prospective imaging data among several different patient populations (125, 126). The interest in this type of imaging data has resulted in a growing set of methods for dealing with longitudinal data, including subtraction imaging (see Fig. 7), our own time series analysis (see Fig. 8), etc. For example, in a study of multiple sclerosis patients (an interesting possible archetype for HIV-associated neurodegeneration) the level of...

Balo Concentric Sclerosis BCS

Figure 12 (See color insert.) Spectrum of inflammatory demyelinating diseases. Marburg type multiple sclerosis Macroscopically, confluent lesions lead to mass effect and herniation (A and B). Microscopically, there is extensive demyelination and axonal loss (C, LFB PAS D, Bielschowsky). Balo concentric sclerosis Note the characteristic alternating bands of demyelination and preserved myelin (E). ADEM The lesions are characterized by perivascular inflammation and only minimal, mainly perivenular demyelination (circles, F). Tumefactive lesion Note with severe edema and mass effect (G). Creutzfeld-Peters cell The presence of these cells should prompt consideration of an active demyelinating lesion (H). Abbreviations LFB PAS, luxol fast blue periodic acid schif ADEM, acute disseminated encephalomyelitis. Source From Ref. 163. Figure 12 (See color insert.) Spectrum of inflammatory demyelinating diseases. Marburg type multiple sclerosis Macroscopically, confluent lesions lead to mass effect...

Discussion and conclusions

Twenty years after its discovery, HHV-6 is an emerging pathogen with an increasing body of data to support disease associations spanning the self-limiting rash of childhood to the ravages of multiple sclerosis. Applying scientific rigor to assessing these associations will be necessary to verify the etiology of these diseases particularly those like fibromyalgia, which remains very difficult to diagnose. The development of additional immunological research tools (both cellular and humoral) as well as molecular, which can also distinguish variants A and B will be synergistic to scientific discovery while providing future tools for monitoring the efficacy of therapy, whatever is the eventual target of treatment. By virtue of its dual tropisms for lymphocytes and nervous tissue, HHV-6 is one of a growing list of viruses, which present both the research challenge and excitement of bridging two important disciplines immunology and neurobiology. This critical connection has enormous...

HHV6 infection of the central nervous system

(AIDS) patients with areas of demyelination (Knox and Carrigan, 1995) and associated with multiple sclerosis (MS) (Akhyani et al., 2000 Kim et al., 2000 Soldan et al., 2000 Rotola et al., 2004). This chapter will focus on evidence suggesting an association of HHV-6 with four major disorders of the CNS childhood febrile seizures, mesial temporal-lobe epilepsy (MTLE), MS, and progressive mul-tifocal leukoencephalopathy (PML).

The association of HHV6 with MS

To extend the observation of cell-free serum HHV-6 DNA in MS patients, a longitudinal study consisting of 215 samples obtained from 59 MS patients followed prospectively for a 5-month period of time was conducted (Berti et al., 2002). Serum HHV-6 DNA was detected from significantly fewer sera obtained during periods of clinical remission. These data suggest a statistically greater likelihood of detecting HHV-6 DNA in the serum of an MS patient during an exacerbation (Berti et al., 2002). This report supports a role for HHV-6 in the pathogenesis of MS by suggesting that the presence of serum HHV-6 DNA, similar to the presence of gadolinium-enhancing lesions, coincides with clinical worsening in a subset of patients (Berti et al., 2002). Additional studies have demonstrated that HHV-6A active replication is associated with a subset of relapsing-remitting multiple sclerosis (RRMS) patients and that HHV-6A active infection increases the risk of exacerbations in these patients...

Upper Motor Neuron Disease

The apt expression jiggling describes a mixed spasticity and cerebellar ataxia and is most frequently seen in patients with multiple sclerosis. The intention tremor of the lower limbs as each foot comes down to the floor plus the stiffness results in a whole body movement that is a fine tremble or jiggle, mostly in the vertical dimension.

Relationship to White Matter Physiology Pathology

The applications of DTI are rapidly growing, in part because the diffusion tensor is exquisitely sensitive to subtle changes or differences in tissue at the microstructural level. DTI studies have found differences in development (e.g., Barnea-Goraly et al. 2005 Snook et al. 2005) and aging (e.g., Abe et al. 2002 Pfefferbaum et al. 2005 Salat et al. 2005), and across a broad spectrum of diseases and disorders including traumatic brain injury (diffuse ax-onal injury) (Werring et al. 1998 Salmond et al. 2006), epilepsy (Concha et al. 2005a), multiple sclerosis (Cercignani et al. 2000 Rovaris et al. 2002 Assaf et al. 2005), ALS (Ellis et al. 1999 Jacob et al. 2003 Toosy et al. 2003), schizophrenia (Buchsbaum et al. 1998 Lim et al. 1999 Agartz et al. 2001 Jones et al. 2006), bipolar disorder (Adler et al. 2004 Beyer et al. 2005), OCD

Relationship to Behavioural and Neural Functioning

As for FA, MTR is a non-specific marker of neural damage, such as demyelina-tion. Many of the published MT studies have focused on patients with multiple sclerosis, who show decreased MT in both ROI and whole-brain histogram analyses. In other diseases, results are similar, indicating MTR is a viable marker for affected white and gray matter. MTR has been shown to increase with brain development during the first several years of life (Rademacher et al. 1999 van Buchem et al. 2001) and regional decreases with aging have been found (Armstrong et al. 2004). Differences in MTR were sufficiently large to distinguish patients with mild cognitive impairment from patients with Alzheimer's disease and controls (Kabani et al. 2002a Kabani et al. 2002b). A number of published studies have also used magnetization transfer methods to compare the brains in patients with schizophrenia against healthy control subjects (Foong et al. 2001 Bagary et al. 2003 Kiefer et al. 2004 Kubicki et al. 2005)....

Magnetization Transfer MRI

MRI pulse sequences can also be specified so as to reduce the signal sensitivity to both T1 and T2 effects by specifying a long TR (to minimize T1 signal differences) and a short TE (to minimize T2 signal differences). The resulting images are sensitive to differences in the overall density of protons within different brain locations. Proton density images can contain information about proton density within fluid relative to macromolecular brain structure (i.e., neural tissue membranes) through the application of an RF pulse which saturates protons in macromolecular brain structures. Magnetization transfer imaging (MTR) then compares sequential proton density images with and without the additional saturating RF pulse to identify alterations in neurochemical (macromolecular) integrity within hard neural tissue, such as white matter plaques in multiple sclerosis or prolactin-secreting tumors versus non-secreting adenomas (Argyropoulou et al, 2003 Zackowski et al, 2009).

Neuroprotectant Properties

Collectively, these results indicate that TDZDs can be very effective neuroprotective and anti-inflammatory compounds in neuronal cells through, at least in part, activation of the nuclear receptor PPARy. This study suggests possible therapeutic uses for TDZDs in certain brain disorders, such as multiple sclerosis, as well as Parkinson's and Alzheimer's diseases, where inflammatory responses play a major role.

Surgical Complications

Surgical complications are those that occur within 30 days of surgery. These complications are typical of those seen with other intracranial stereotactic procedures and generally occur in less than 5 of the patients. These complications include hemorrhage, ischemic lesions, seizures, infections, and misplaced leads. Several studies have focused on the examination of surgical complications related to DBS. Beric et al. (46) reported 86 patients who received 149 DBS implants in the VIM nucleus of the thalamus, GPi or STN for PD, essential tremor, multiple sclerosis, or dystonia. In this cohort, 2.3 (n 2) of the patients had a hemorrhage, 2.3 (n 2) had seizures, 1.2 (n 1) had a delayed hematoma two months after surgery, and 4.7 (n 4) had postsurgical confusion. Umemura et al. (47) reported surgical complications in 109 patients receiving DBS of the VIM nucleus of the thalamus, GPi, STN, or anterior nucleus of the thalamus for PD, essential tremor, epilepsy, or dystonia. They reported two...

Hardware Related Complications

Several reports have also focused on hardware complications related to DBS. Beric et al. (46) examined complications for 86 DBS patients and found electrode failure in 3.5 (n 3), extension wire failure in 4.7 (n 4), IPG malfunction in 1.2 (n 1), and pain at the IPG in 1.2 (n 1). Kondziolka et al. (49) examined hardware complications in 66 patients undergoing unilateral thalamic DBS for either essential tremor, parkinsonian tremor, multiple sclerosis, or other forms of tremor. There were a total of 23 hardware-related complications affecting 27 of the patients. Lead breakage occurred in 10 patients (15.2 ), system infection in seven patients (10.6 ), connector erosion in two patients (3.0 ), and cranial lead migration, chronic subdural hematoma, defective IPG, and a defective connector each in one patient (1.5 , each). Oh et al. (50) reported hardware complications for 79 patients who received 124 DBS implants. DBS was done for PD, essential tremor, pain, epilepsy, dystonia, multiple...

Brief Review Of Basic Aspects Of Nonconventional Mr Techniques

Figure 3 Axial magnetic resonance images from a patient with multiple sclerosis. The proton density weighted scan (A) shows multiple lesions. On the scalp-stripped magnetization transfer ratio map (B), lesions appear as hypointense areas. The degree of hypointensity is related to decrease in magnetization transfer ratio and indicates damage to myelin and to axonal membranes. Figure 3 Axial magnetic resonance images from a patient with multiple sclerosis. The proton density weighted scan (A) shows multiple lesions. On the scalp-stripped magnetization transfer ratio map (B), lesions appear as hypointense areas. The degree of hypointensity is related to decrease in magnetization transfer ratio and indicates damage to myelin and to axonal membranes. Figure 4 Axial magnetic resonance images from a patient with multiple sclerosis. (A) Proton density-weighted image. On the scalp-stripped mean diffusivity map (B), some of the lesions appear as hyperintense areas. The degree of hyperintensity...

The Role Of Mri In The Diagnosis And Prognosis Of Ms

Figure 6 Axial fast-fluid-attenuated inversion recovery images (A and B) from a patient with multiple sclerosis. In (A) and (B), multiple sclerosis lesions appear as areas of increased signal. The suppression of the signal of the cerebrospinal fluid allows a better identification of the lesions located in the periventricular and juxtacortical regions. Figure 6 Axial fast-fluid-attenuated inversion recovery images (A and B) from a patient with multiple sclerosis. In (A) and (B), multiple sclerosis lesions appear as areas of increased signal. The suppression of the signal of the cerebrospinal fluid allows a better identification of the lesions located in the periventricular and juxtacortical regions. Figure 7 Axial proton density-weighted (A) and postcontrast (Gd DTPA, 0.1 mmol kg) T1-weighted (B) magnetic resonance images of the brain from a patient with multiple sclerosis. In (B), two patterns of enhancement are visible a homogeneous one (indicating newly formed lesions) (continuous...

The Role Of Mri In Understanding Ms Pathophysiology

Figure 12 Relative cortical activations on a rendered brain during the performance of a simple motor task with the dominant, functionally unaffected right hand in patients with clinically isolated syndromes suggestive of multiple sclerosis who evolved to definite multiple sclerosis over a short-term follow-up period (A and B) compared with those who did not (C and D). When compared with (C and D), in (A and B), a more extensive and widespread activation of the sensorimotor network is visible. Figure 12 Relative cortical activations on a rendered brain during the performance of a simple motor task with the dominant, functionally unaffected right hand in patients with clinically isolated syndromes suggestive of multiple sclerosis who evolved to definite multiple sclerosis over a short-term follow-up period (A and B) compared with those who did not (C and D). When compared with (C and D), in (A and B), a more extensive and widespread activation of the sensorimotor network is visible....

The errorrelated negativity ERN

For clinical purposes, sensory evoked potentials are used in the diagnosis of neurological diseases (i.e., demyelinat-ing diseases, cerebral tumors and infarctions, etc.). Of particular diagnostic importance are the auditory brainstem potentials (diseases involving the posterior fossa), and the steady-state visual potential (multiple sclerosis). Auditory potentials can also be used to diagnose hearing defects in uncooperative subjects (such as newborn infants). Because most sensory potentials appear to be insensitive to psychological factors, they have not been used extensively in the study of psychological processes.

Interactions Between Medical Illness and Psychiatric Symptoms Longitudinally

For many such illnesses, including MS, IBD, sickle cell, and others, these relapses are associated with significant increases in psychiatric symptoms such as depression and anxiety (Dalos et al, 1983 Graff et al, 2009 Levenson et al, 2008), which can result in a unique set of disease-related effects on psychiatric outcomes in an RCT (see arrow (d)). MS is a good example of this phenomenon. Multiple sclerosis is in part an autoimmune disease in which many patients experience sudden exacerbations or increases in inflammation and symptoms that can last a period of weeks or months. During disease exacerbation, distress may be experienced by as many as 90 of patients (Dalos et al, 1983). Depression in MS may be due in part to the increased inflammation and cytokine production that are part of the patho-genesis of multiple sclerosis (Gold and Irwin, 2006). Furthermore, these exacerbations are most commonly treated with high-dose infusions

Lieve Naesens Leen De Bolle Erik De Clercq

In contrast to other human herpesviruses such as herpes simplex virus (HSV) or cytomegalovirus (CMV), HHV-6 has not been the subject of extensive antiviral screening, the main reason being the uncertainty about the large need for specific anti-HHV-6 therapies. Transplant recipients commonly show laboratory signs of HHV-6 reactivation, but the frequency by which this is associated with serious disease is still ill defined (Yoshikawa, 2004). Even more controversial is the role of HHV-6 in chronic neurological disorders, such as multiple sclerosis (MS) or chronic fatigue syndrome (CFS). In the absence of HHV-6-specific therapies, treatment of HHV-6 infections currently relies on the relatively broad-spectrum antiherpetic agents (val)ganciclovir and foscarnet. Although these drugs offer an indisputable benefit in the therapy or prophylaxis of CMV, their clinical efficacy against HHV-6 can only be estimated from a number of heterogeneous case reports. Long-term administration of these...

History of Response Shift

In the 1990s, interest in response shift developed in studying QOL. Clinicians began to recognize that response shift could obfuscate important treatment-related changes and indeed might even be the subtext or the desired effect in rehabilitation and psychosocial interventions (Schwartz and Sprangers, 1990 Schwartz et al, 1999, 2007). Response shift has now been studied and recognized to affect adaptation to a wide degree of health conditions, including multiple sclerosis (Christensen et al, 1999 Brandtstadter and Renner, 1990 Helson, 1964 Schwartz and Sendor, 1999), cancer (Ahmed et al, 2009a Bernhard et al, 1999, 2001 Boyd et al, 1990 Breetvelt and Van Dam, 1991 Cella et al, 2002a Hagedoorn et al, 2002 Jansen et al, 2000 Kagawa-Singer, 1993 Oort et al, 2005 Schwartz et al, 1999 Sprangers et al, 1999), stroke (Ahmed et al, 2003, 2004, 2005), diabetes (Li and Rapkin, 2009 Postulart and Adang, 2000), geriatrics (Daltroy et al, 1999 Rapkin, 2009), palliative care (Schwartz et al, 2002,...

Affected Organs And Cell Types In Polyomavirusassociated Disease And Persistent Virus Infection

To analyze the role of CNS diseases other than PML in the activation of renal JCV infection, viruria was studied in a group of patients with multiple sclerosis (MS). PCR analysis revealed an excretion rate of 30-41 in chronic progressive MS (Agostini et al., 2000 Stoner et al., 1998). Because a control group of family members exhibited the same excretion rate, a regular influence of MS on JCV renal infection is rather unlikely. In conclusion, it can be as

Mechanisms of Recovery

Figure 15 Sagittal diffusion tensor magnetic resonance image of the cervical cord from a patient with relapsing-remitting multiple sclerosis mean diffusivity map (A), fractional aniso-tropy map (B), and color-encoded map of directionality (dark gray color means a preferential fiber direction along the z-axis, gray color along the x-axis, light gray color along the y-axis). The loss of normal fiber directionality is visible (C). Figure 15 Sagittal diffusion tensor magnetic resonance image of the cervical cord from a patient with relapsing-remitting multiple sclerosis mean diffusivity map (A), fractional aniso-tropy map (B), and color-encoded map of directionality (dark gray color means a preferential fiber direction along the z-axis, gray color along the x-axis, light gray color along the y-axis). The loss of normal fiber directionality is visible (C). Table 3 Main Damaging Recovery Aspects of Multiple Sclerosis and Magnetic Resonance Imaging Techniques with the Potential to Provide...

Mri In Monitoring Treatment Efficacy In Ms Trials

Figure 17 (A) Scatterplot of the correlation between the relative activation of the contralateral primary sensorimotor cortex and average lesion mean diffusivity in nondisabled relap-sing-remitting multiple sclerosis patients during a simple motor task. (B) Scatterplot of the correlation between the relative activation of the contralateral infraparietal sulcus and normal appearing brain tissue average mean diffusivity in nondisabled relapsing-remitting multiple sclerosis patients during a simple motor task. Figure 17 (A) Scatterplot of the correlation between the relative activation of the contralateral primary sensorimotor cortex and average lesion mean diffusivity in nondisabled relap-sing-remitting multiple sclerosis patients during a simple motor task. (B) Scatterplot of the correlation between the relative activation of the contralateral infraparietal sulcus and normal appearing brain tissue average mean diffusivity in nondisabled relapsing-remitting multiple sclerosis patients...

Some Diseases Of The Visual System Retina and Optic Nerve Lesions

There may be a past history of episodes of multiple sclerosis or this illness may be the first manifestation of it. The fundus is usually normal. Afferent pupillary defect is commonly present. Be careful and persistent with patients with visual loss. Lesions in the chi-asmal region can be deceptive and extremely chronic. The chronicity and slow progression seem to make the symptoms more acceptable and less demanding. Every neurologist and neurosurgeon has had some bad experience with patients thought to have multiple sclerosis, amblyopia from childhood, low-tension glaucoma, retinitis pigmentosa sine pigmento, or atypical macular degeneration as an explanation for their blindness who eventually turn out to have a chiasmal lesion as the true cause. It does not help the patient to

Arrival Of Pml Cases And An Electron Microscope

Sam (Shi-Ming) Chou joined the Department of Pathology as a postdoctoral student with the aim of completing a Ph.D. program in Zoology and Pathology. Supported by the National Multiple Sclerosis Society, he engaged in research in neurolathyrism. By 1962, he had decided that he would choose neuropathology as his career. He opted to take the course that I gave for the neurology residents.

Neurological Disease And Therapy

Handbook of Multiple Sclerosis, edited by Stuart D. Cook 43. Handbook of Multiple Sclerosis Second Edition, Revised and Expanded, edited by Stuart D. Cook 53. Handbook of Multiple Sclerosis Third Edition, edited by Stuart D. Cook 80. Handbook of Multiple Sclerosis, Fourth Edition, edited by Stuart D. Cook Handbook of Multiple Sclerosis Fourth Edition

HHV6 Genome Similar and Different

Hhv6 Genome

Roseoloviruses, human herpesviruses 6 and 7 (HHV-6, HHV-7) are widespread T lymphotropic and neurotropic viruses causing mostly benign infections. However, particularly for HHV-6, during some primary as well as secondary reactivated infections, which can follow immune aberrations or deficiencies, there can be severe complications which can lead to fatalities. Thus, this is of relevance for immuno-suppressed HIV AIDS or transplantation patients, as well as increasingly, for those with neurological disease, including encephalitis and a link with multiple sclerosis (primarily HHV-6A). Understanding when and how this virus does or does not cause disease is key to developing effective treatments plus evaluating the impact of HHV-6 infections on worldwide populations. Studies on the virus genome provide a foundation for this exploration and can guide the way towards development of new anti-virals as well as possible novel treatments for immune-related pathologies using this well-adapted...

Noninsulindependent Type II diabetes mellitus

A full account of the natural selection pressures in relation to NIDDM remains elusive. However, it is near certain that critical variations in dietary circumstances, over time, have evolution-arily shaped the pattern of differences in metabolic handling of dietary substrates. Viewed within this frame, environment is a formative influence on the human genotype. The complex dependence of immune system development and functioning on vitamin D synthesis and action may be another such example. This is illustrated by the epidemiology of multiple sclerosis, with its evidence of both environmental and genetic influences on aetiology.

Current immunological tools

Disease associations between HHV-6 infection and multiple sclerosis, fibromyalgia, and chronic fatigue syndrome Ablashi et al. (2005) have performed a meta-analysis of over 85 published papers in which the relationship between HHV-6 and patients with multiple sclerosis or fibromyalgia, or chronic fatigue syndrome (CFS) was examined. Although a clear causal relationship has not been established between HHV-6 and these chronic illnesses, his study discerned that there is evidence of correlation in more than 75 of those papers that distinguish between active and latent virus. Since both in vitro studies and in vivo clinical experience provide evidence that HHV-6 is immuno-suppressive, patients with a history of CFS (data provided through the courtesy of Daniel Peterson, MD) were tested for the functionality of their global T-cell response using an FDA-cleared test for cell-mediated immunity assessment (Cylex Immune Function Assay, ImmuKnowTM) and these cellular immune responses were...

Jeanmartin Charcot And The Salpetriere School

FIGURE 16 Charcot's early tremor recordings. Charcot adapted the sphygmograph, an instrument originally used for recording arterial pulsation, to record tremors and movements of the wrist. His resultant tremor recordings (lower right), conducted at rest (A-B) and during activity (B-C), differentiated multiple sclerosis (top recording) from the pure rest tremor (lower recording) or mixed tremor (middle recording) of Parkinson's disease (19). FIGURE 16 Charcot's early tremor recordings. Charcot adapted the sphygmograph, an instrument originally used for recording arterial pulsation, to record tremors and movements of the wrist. His resultant tremor recordings (lower right), conducted at rest (A-B) and during activity (B-C), differentiated multiple sclerosis (top recording) from the pure rest tremor (lower recording) or mixed tremor (middle recording) of Parkinson's disease (19).

Cellular homologues

U83 encodes a functional chemokine (Zou et al., 1999). Although the gene has relatively little sequence similarity to human chemokine genes, the protein expressed has the typical cysteine residues of a chemokine, transduces signals that involve calcium fluxes and induces chemotactic activation. The recombinant U83 protein is capable of inducing transient calcium mobilization in THP-1 cells and of chemotactically activating THP-1 cells (Zou et al., 1999). Furthermore, the U83 has been found to cause calcium mobilization as efficiently through the CCR2 receptor (Luttichau et al., 2003), suggesting that the U83 protein might play an important role in HHV-6 propagation in vivo by activating and trafficking mononuclear cells to sites of viral replication, or U83 during reactivation of the virus in for example monocyte-derived microglia could perhaps be involved in the pathogenesis of the CCR2-dependent disease, multiple sclerosis.

Surprises

About a month after our first successful isolation of virus from J.C. brain tissue, Gabriele received a telephone call from Richard Johnson at Johns Hopkins Medical School. He invited her to attend a workshop on the epidemiology of multiple sclerosis at Easton, Maryland, and to visit his laboratory where she ''would be able to see the virus of PML.'' After Gabriele conveyed this news to me I talked by phone with Johnson and learned that Leslie Weiner and he had a papova-like agent growing in primary African green monkey kidney cells. They had made isolations from two cases of PML using cell fusion and co-cultivation techniques. Just the fact that their isolates grew well in green monkey kidney cells made it unlikely that their virus was the same as ours. I told him we had an isolate also, and he and I agreed that Gabriele and Billie both should attend the workshop so their isolates and ours could be compared.

Neuroimaging

Neuroimaging has provided insight into the pathophysiology and natural history of Parkinson's disease (PD) and has emerged as a tool to monitor disease progression and to assess new potentially neuroprotective or neurorestorative therapies for PD. Diverse imaging methods have been successfully applied to neurological disorders. Although technology such as functional magnetic resonance imaging or magnetic resonance spectroscopy has been especially useful in assessing stroke, multiple sclerosis, and epilepsy (1-3), in vivo neuroreceptor imaging using single photon emission tomography (SPECT) and positron emission tomogrpahy (PET) have so far been most valuable in assessing PD. SPECT and PET use specific radioactively labeled lig-ands to neurochemically tag or mark normal or abnormal brain chemistry. Recent advances in radiopharmaceutical development, imaging detector technologies, and image analysis software have expanded and accelerated the role of imaging in clinical research in PD,...

MRI Segmentation

MRI is one of the most common diagnostic tools in neuroradiology. In brain pathology study, brain and brain tissues have often regions of interest from which abnormality such as the Alzheimer disease or multiple sclerosis (MS) lesions are diagnosed. Numerous techniques in computer-aided extraction of the brain, brain tissues, such as the gray matter, white matter, and cerebrospinal 6.4.1.2 Segmentation of Lesions in Multiple Sclerosis from MRI

Organic Disorders

Organic brain disorders are either acute or chronic. Acute brain dysfunctions can result from myriad conditions alcohol intoxication, anemia, brain tumors, cardiovascular disorders, emphysema, fever, infections, infectious diseases, lead poisoning, liver disease, medication, mercury poisoning, multiple sclerosis, stroke, thyroid disorders, and vitamin deficiencies. The two most common chronic brain disorders Alzheimer's disease and multi-

Clinical Studies

Magnetic resonance imaging (MRI) is frequently used to document in vivo neuropathology in humans, such as stroke, multiple sclerosis and Alzheimer's disease. However, this imaging technology has also been applied to human aging studies, in both cross-sectional and longitudinal designs. The utility of repeated imaging is that each individual serves as his or her own baseline, avoiding many of the pitfalls of cross-sectional studies (secular trends). In general, these studies have concentrated on the evaluation of dual-echo or 3-dimensional scans generated by MRI sequences (SPGR, MPRAGE), which yield high-resolution images that can be used to measure total brain volume or segmented into various tissue compartments (gray, white, cerebrospinal fluid) or specific anatomical regions.

The Active MS Lesion

Figure 2 (See color insert.) Active multiple sclerosis lesion. Active lesions are hypercellular demarcated regions of myelin loss characterized by an admixture of macrophages and reactive astrocytes (A, LFB PAS). Creutzfeld-Peters cells are astrocytes containing fragmented nuclei that resemble astrocytic mitoses (arrows A and B, H&E). Abbreviation LFB PAS, luxol fast blue periodic acid schif. Figure 2 (See color insert.) Active multiple sclerosis lesion. Active lesions are hypercellular demarcated regions of myelin loss characterized by an admixture of macrophages and reactive astrocytes (A, LFB PAS). Creutzfeld-Peters cells are astrocytes containing fragmented nuclei that resemble astrocytic mitoses (arrows A and B, H&E). Abbreviation LFB PAS, luxol fast blue periodic acid schif.

Late Remyelination

Figure 7 (See color insert.) Remyelination in chronic multiple sclerosis is characterized by the reduced staining intensity of myelin and may be restricted to the lesion edge (A MBP) or present throughout the lesion (B, shadow-plaque LFB PAS). Abbreviation LFB PAS, luxol fast blue periodic acid schif. Source From Ref. 163. Figure 7 (See color insert.) Remyelination in chronic multiple sclerosis is characterized by the reduced staining intensity of myelin and may be restricted to the lesion edge (A MBP) or present throughout the lesion (B, shadow-plaque LFB PAS). Abbreviation LFB PAS, luxol fast blue periodic acid schif. Source From Ref. 163.

Conclusions

Each other and regulate the transcription of JCV. In addition, chromatin structure and DNA methylation might be other factors controlling cell-specific expression. In the future, identification of novel aspects of JCV neurotropism should shed light not only on our understanding of the biochemical mechanism of virus infection, but also on the therapy of glial-specific diseases such as PML, multiple sclerosis, and other demyelinating diseases.

Pathological Studies

Figure 10 (See color insert.) Axon loss in multiple sclerosis. Axonal density is reduced at the plaque edge and the plaque center, relative to the PPWM (A neurofilament protein). Some of the reduced neurofilament staining at the active plaque edge can be attributed to macrophage infiltration. Consistent with acute axonal injury are numerous enlarged axonal profiles, axonal spheroids, and fragmented axons within the lesion (B, amyloid precursor protein C, Bielschowsky silver). Abbreviation PPWM, periplaque white matter. Figure 10 (See color insert.) Axon loss in multiple sclerosis. Axonal density is reduced at the plaque edge and the plaque center, relative to the PPWM (A neurofilament protein). Some of the reduced neurofilament staining at the active plaque edge can be attributed to macrophage infiltration. Consistent with acute axonal injury are numerous enlarged axonal profiles, axonal spheroids, and fragmented axons within the lesion (B, amyloid precursor protein C, Bielschowsky...

Judith A Britz

Fibromyalgia, chronic fatigue syndrome (CFS), and potentially multiple sclerosis. As molecular, serological, and cellular methodologies for HHV-6's detection improve, insight into causality will provide avenues for developing prophylactic and treatment strategies for this ubiquitous virus that affects millions of individuals.

Interferons

The Food and Drug Administration (FDA) has recently approved the use of interferons to treat a number of diseases. Alpha interferon, for example, is now being used to treat hepatitis C, hairy-cell leukemia, virally induced genital warts, and Kaposi's sarcoma. The FDA has also approved the use of beta interferon to treat relapsing-remitting multiple sclerosis and the

Voiding symptoms

LUTS are a feature in women with urethral stenosis or obstruction of the urethra by a gravid uterus or severe genital organ prolapse. Failure of the normal sphincter mechanisms to relax and open during voiding will lead to voiding symptoms. This is seen after spinal trauma and in some patients with multiple sclerosis.

Acknowledgements

The authors would like to thank Mariana Lazar, Yu-Chien Wu, Alexey Samsonov, Yijing Wu, and Aaron Field at the University of Wisconsin for providing figures, as well as Steve Smith from Oxford and Greg Stanisz from Sunnybrook Health Sciences Centre, and thanks also to Ana Solodkin at the University of Chicago for lively discussions. Some of the diffusion MRI work presented here was supported by NIH grant RO1 MH 62015 and the MT and MWF data was generated from a grant from the National Multiple Sclerosis Society (University of Wisconsin).

Chelation

Chelation is typically used as an intravenous therapy (sometimes oral) to remove a particular substance that is found to occur at a toxic level in the body such as lead, copper, mercury, or arsenic. The amino acid complex, ethylene-diamine-tetra-acetic acid, is the most commonly used chelating agent, though herbs and supplements may sometimes be used. Though there is a higher incidence of PD occurring in persons with chronic exposure to heavy metals such as manganese and copper and also with exposure to pesticides and herbicides, no specific toxic agent directly linked to the cause of PD has ever been identified and it is unclear what one would attempt to chelate out of the body of someone with PD. There is no scientific evidence to support the use of chelation therapy for the treatment of PD. In fact, chela-tion therapy has come under investigation and criticism for making false statements about its curative powers for a number of diseases such as multiple sclerosis, Alzheimer's...

A5021 297

CNS demyelination 312-6 febrile seizures 214-5 HHV-6 infection 213-4, 215, 257f mesial temporal-lobe epilepsy (MTLE) 215 multiple sclerosis (MS) 215-8 progressive multifocal leukoencephalopathy (PML) 219-20 cerebral lymphomas 194 characteristic tissue reaction 140f chronic allograft nephropathy 205, 286 chronic fatigue syndrome (CFS) 86-7, 207-9, 251-2, 309

Marburg MS

The Marburg variant of MS, recognized as a fulminant and lethal subtype of multiple sclerosis by Otto Marburg in 1906 (138), is characterized by rapid progression and an exceptional severity. The course is generally monophasic and relentlessly progressive, with death consequent to brainstem involvement or mass effect with herniation. Peripheral nervous system involvement may also occur in this variant of MS. Pathologically, the lesions are more destructive than typical MS and characterized by a large confluent area of white matter destruction with massive macrophage infiltration, pronounced acute axonal injury, and frank tissue necrosis (Figure 12). Uncommonly, multiple small lesions may be disseminated throughout the brain and spinal cord, or may coalesce to form large confluent areas of destruction. In some cases, areas of remyelination are observed. An autopsied case of Marburg disease documented pronounced post-translational changes, in which MBP was converted to an extensively...

Types of MS Lesions

Figure 4 (See color insert.) Types of multiple sclerosis plaques (KiMlP, macrophage marker). (A) Acute active multiple sclerosis plaques are characterized by extensive macrophage infiltration throughout the extent of the lesion with macrophages containing both early and late myelin degradation products. (B) The radially expanding active rims consist of macrophages containing early and late myelin degradation products clustered at the advancing edge of the plaque, and diminishing in number towards the inactive plaque center. (C) Smoldering plaques are characterized by a low grade of demyelinating activity at the plaque edge, with very few macrophages containing myelin degradation products. (D) The inactive plaque is hypocellular and contains no early or late myelin degradation products within the macrophages. Figure 4 (See color insert.) Types of multiple sclerosis plaques (KiMlP, macrophage marker). (A) Acute active multiple sclerosis plaques are characterized by extensive macrophage...

Fatigue

The neurologic disorder in which fatigue has been best evaluated is multiple sclerosis in which at least 78 of these patients suffer from fatigue and is often the most disabling symptom of this disease (55). Similarly, in a study of over 1300 cancer patients, 58 of patients described problems with fatigue, yet less than 52 of those ever reported symptoms to their caregivers, and only 14 had received some type of treatment (56). Perhaps the greatest obstacle to recognizing fatigue is in terms of definition as various health care professionals define fatigue differently based on their area of expertise. The most common complaint heard in our outpatient brain tumor clinic on a daily basis from patients, regardless of stage of treatment, is that they feel fatigue. This may be further defined as tiredness, exhaustion, muscle weakness, lethargy, or depression. Because fatigue can mean different things to physicians and patients it is imperative that the physician obtain a comprehensive...

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