Objective
The aim of this study was to assess the potential impact of effort in comparative studies assessing NeuroCognitive Dysfunction in patients with and without a Neurologic diagnosis.

Background
It was hypothesized that a subgroup within a group of patients with prominent NeuroCognitive complaints but without a Neurologic diagnosis would have impaired performance on a task originally designed to detect Malingering.

Method
We compared the NeuroPsychological performance of a group of 40 patients with a definite diagnosis of Multiple Sclerosis (MS) with that of 67 patients with Chronic Fatigue Syndrome (CFS).

The Amsterdam Short-Term Memory Test, a Forced-Choice Memory Task, served as measure to detect submaximal effort. In addition, we administered a regular NeuroPsychological task generally considered to be sensitive for Cognitive deterioration.

Results
Compared with the MS group (13%), a larger proportion of the matched CFS group (30%) obtained scores indicative of reduced effort.

In contrast, the proportions of patients scoring below the cutoff value on a conventional NeuroPsychological test did not differ significantly (17% of MS patients and 16% of CFS patients).

Conclusions
The results obtained raise the question of to what extent abnormal test findings in the absence of documented Neurologic Impairment should be interpreted as a sign of Cerebral Impairment.

The suggestion has been made to screen more often for biased results in comparative research studies so as to enhance valid interpretation of NeuroPsychological findings.

High-dose IntraVenous ImmunoGlobulin (IVIg) treatment has become a promising Immune therapy that can modulate the Immune System at several levels, including the Complement cascade.

In relation to Inflammatory DeMyelinating Disease, there is some clinical evidence for the suppression of disease activity by IVIg, while a role in promoting ReMyelination after experimental Myelin damage has been described.

AntiBody and Complement deposition have been implicated in the Immune attack in some cases of Multiple Sclerosis (MS).

We studied the effect of IVIg using the model of Complement-mediated cell injury on Oligodendroglia in vitro, to investigate the mechanisms of action of IVIg.

There was no effect on direct Complement Lysis of the OligodendroGlial Cell line CG4, but AntiBody-dependent Complement damage was inhibited in a dose-dependent manner by IVIg.

These results were confirmed with Primary cultures of Oligodendrocyte Precursor cells (OPC) and Oligodendrocytes.

The addition of excess C1, C3, and C4 did not influence the inhibitory effect of IVIg, implying that binding of these Complement components does not play a role, in contrast to other experimental models of Complement damage.

F(ab')2 ImmunoGlobulin fragments were at least partially responsible for the effect.

We conclude that IVIg may be protective in AntiBody-mediated Complement injury of Oligodendrocytes and their Progenitors, and that this effect is likely to be mediated via AntiBody binding, rather than interference with Complement activation.

Inhibition of Inflammatory mechanisms, as opposed to a direct effect on ReMyelinating Cells, may underlie the role of IVIg in promoting Myelin repair in experimental models.

Objective
To determine the prevalence of Depression in Multiple Sclerosis in the community and to assess how the presence of Depression affects patients' perception of their Disability.

Design, Setting & Subjects
Consecutive case series. The study was carried out at a regional Multiple Sclerosis (MS) clinic, in eighty-eight patients with MS.

Main Outcome Measures
Patients were asked to complete the following questionnaires: Hospital Anxiety and Depression Scale (HADS), Beck Depression Inventory (BDI), Rankin Scale of Disability/Handicap (completed by patient and physician to assess relative perceived Disability) and two Visual analogue scales (coping ability and perceived service adequacy).

Results
Thirty-nine per cent were case level for Depression using the BDI criteria of Sullivan; 17% were case level for Depression (34% borderline case) and 34% case level for Anxiety on HADS.

Depressed patients using both BDI and HADS criteria were three times more likely than nondepressed patients to perceive their Disability as being greater than the physicians' perception (p < 0.001).

Conclusion
Depression is common in MS and adversely affects patients' perception of their Disability.

Survival to 1996 was analyzed for nearly 2500 veterans of World War II who were rated as 'service-connected' for Multiple Sclerosis as of 1956 by the then Veterans Administration.

Survival from onset was defined for all white women and black men, and a random sample of white men. Median survival times from onset were 43 years (white females), 30 years (black males) and 34 years (white males).

Crude 50-year survival rates were 31.5% (white females), 21.5% (black males) and 16.6% (white males), but only the white females and white males were significantly different.

A proportional hazard analysis was used to identify risk factors for mortality from Multiple Sclerosis onset year.

Significant risk factors included male sex (risk ratio: 1.57), older age at onset (risk ratio: 1.05 per year) and high socioeconomic status (risk ratio: 1.05 per socioeconomic status category).

There were no statistically significant differences in survival following Multiple Sclerosis onset by race or latitude of place of entry into military service, both significant risk factors associated with the development of Multiple Sclerosis.

Standardized mortality ratios utilizing national US data (for 1956-96) showed a marked excess for all three race-sex groups of Multiple Sclerosis cases, with little difference among them, but with a decreasing excess over time.

Relative survival rates, used to compare the survival of Multiple Sclerosis cases with that of other military veterans, did not differ significantly by sex-race group, nor by latitude of place of entry into military service, but did differ significantly by SocioEconomic class.

The lack of difference in male and female relative survival rates suggests that the significant difference in survival between male and female Multiple Sclerosis cases is, at least in part, a result of sex per se and not the disease.

To investigate Visual Signal Processing in patients with Optic Neuritis, suspected Multiple Sclerosis, confirmed Multiple Sclerosis (MS), and Optic Neuritis combined with MS, pattern reversal Visual Evoked Potentials (VEPs) were recorded in patients and normal subjects.

The amplitude and latency of the first positive peak, P100 were determined to assess Electrical Conduction in patients as compared to normal subjects. Suspected MS patients did not differ from normal subjects in peak latencies or amplitudes.

The P100 amplitude was reduced in Optic Neuritis, confirmed MS and Optic Neuritis combined with confirmed MS.

The P100 and N145 latencies were prolonged in Optic Neuritis patients and confirmed MS patients as compared to normal subjects.

The main characteristic of Optic Neuritis was P100 amplitude reduction, and of confirmed MS was P100 latency delay. There was a progression of the P100 latency delay and of the P100 amplitude decrement in Optic Neuritis, confirmed MS, and Optic Neuritis combined with confirmed MS.

These results indicate a progression of DeMyelination in Optic Neuritis, confirmed MS, and Optic Neuritis combined with confirmed MS.

Pain is experienced by approximately two-thirds of all people with Multiple Sclerosis (MS) at some time during the course of their disease.

Pain in MS occurs as a consequence of both the disease and the disability that it produces.

Pain in MS is receiving more attention as clinical trials in the past decade have focused not solely on the Immune System modulators of disease but also on symptomatic management as well.

Nurses with their keen communication and assessment skills and their unique advocacy role are particularly equipped to effect Pain Management for people with Multiple Sclerosis.

To assess whether Interferon beta1a (IFN-ß-1a) therapy affects Plasma LipoProtein metabolism, twelve patients with Relapsing/Remitting Multiple Sclerosis (MS) were studied during a two-year follow-up period.

High density LipoProtein (HDL2) Cholesterol and the HDL2/HDL3 ratio were increased at year 2 and LipoProtein (a) was transitorily increased at year 1, in comparison to baseline levels.

ApoLipoProtein A-I was lower and ApoLipoProtein E higher at year 1, only in a subgroup of patients who experienced relapses and/or progressed during therapy.

These findings suggest that IFN-ß-1a treatment is associated with changes in the LipoProtein Metabolism.

Alterations in this metabolism could be related to the ImmunoModulatory actions of the drug and the disease activity in Multiple Sclerosis patients.

Objectives
To measure the effect of Baclofen on the transmission in different Spinal Pathways to Soleus MotoNeurones in Spastic Multiple Sclerosis patients.

Methods
Baclofen was administered Orally in 14 and Intrathecally in 8 patients.

H(max)/M(max), PreSynaptic Inhibition by biceps femoris tendon tap of Femoral Nerve stimulation, depression of the Soleus H-reflex following previous activation of the Ia afferents from the Soleus Muscle (i.e. postactivation depression), DiSynaptic Reciprocal Ia Inhibition of the Soleus H-reflex and the number of backpropagating action potentials in primary afferents, which may be a sign of PreSynaptic Inhibition, were examined.

Results
Baclofen depressed the Soleus H(max)/M(max) ratio significantly following Oral and Intrathecal Baclofen.

None of the two tests of PreSynaptic Inhibition, or the postactivation depression or the DiSynaptic Reciprocal Ia Inhibition of the Soleus H-reflex were affected by Baclofen administration.

Also the Action Potentials of the primary afferents were unchanged during Baclofen administration.

Conclusions
The AntiSpastic effect of Baclofen is not caused by an effect on the transmitter release from Ia afferents or on DiSynaptic Reciprocal Ia Inhibition.

One possible explanation of the depression of the H-reflex by Baclofen is suggested to be a direct depression of MotoNeuronal Excitability.

Stigma of visible and invisible chronic conditions Nurses deliver care to people with various forms of chronic illnesses and conditions.

Some chronic conditions, such as Paraplegia, are visible while others, such as Diabetes, are invisible. Still others, such as Multiple Sclerosis, are both visible and invisible.

Having a chronic illness or condition and being different from the general population subjects a person to possible stigmatization by those who do not have the illness.

Coping with stigma involves a variety of strategies including the decision about whether to disclose the condition and suffer further stigma, or attempt to conceal the condition or aspects of the condition and pass for normal.

We present a beginning framework that describes the relationship between the elements of stigma and the decision to disclose or hide a chronic condition based on its visibility or invisibility.

The specific aims were to combine the results from a meta-study on qualitative research with a review of the quantitative literature, then develop a theoretical framework.

Although an understanding of how patients cope with stigmatizing conditions is essential for nurses who aim to deliver comprehensive individualized patient care, there is little current literature on this subject.

The relationship between visibility and invisibility and disclosure and non-disclosure remains poorly understood. A framework to facilitate a deeper understanding of the dynamics of chronic illnesses and conditions may prove useful for practice.

AutoAntigen-specific T-Lymphocytes are present in patients with AutoImmune Disease and in normal subjects. Little is currently known about the temporal variation (dynamics) of the Immune repertoire of these AutoReactive T-Cells.

We analyzed the long-term variation of the Immune repertoire of T-Cells specific for Myelin Basic Protein (MBP) in five untreated patients with Multiple Sclerosis and four normal control subjects over a mean observation period of 6 years.

MBP-specific CD4⁺ T-Cell lines were selected with purified human MBP, and their Epitope specificity was mapped with overlapping synthetic Peptides. Three distinct patterns of repertoire development were observed.

1. Two patients and three control subjects maintained a broad Epitope response with fluctuations over time.

2. Two patients initially showed a focused response that broadened over the course of 6 years; this finding could be described as intramolecular Epitope spreading.

3. In one patient and one control subject, a strikingly focused response, which was directed to a cluster of nested Epitopes in the MBP region 83-102, persisted over time.

T-Cell receptor Vbeta sequence analysis allowed us to trace individual clones of MBP-specific T-Cells for up to 7 years in the peripheral circulation in four of the five patients and three of the four controls, suggesting that the long-term persistence of MBP-specific T-Cell clones is a common feature of the T-Cell repertoire not unique to Multiple Sclerosis.

The persisting MBP-specific T-Cell clones were not detectable in the blood of one of the patients by Complementarity-determining region (CDR)-3 spectratyping, indicating that their frequency does not exceed 1 in 5000 T-Cells.

The temporal characteristics of the MBP-specific T-Cell repertoire described here are relevant to therapeutic strategies targeting AutoAntigen-specific T-Cells in Multiple Sclerosis and other AutoImmune Diseases.