Psychogenic Movement Disorders: Gait Is a Give-Away!

The aim of this article is to point out that an incongruity of gait disorder (either in relation to the presenting movement disorder or incongruity with any type of organic gait disorder) is a useful clue in diagnosing psychogenic movement disorders. To illustrate this, we present a case series of patients with various types of psychogenic movement disorders (rest tremor, myoclonus, dystonia, and chorea). Incongruity of the walking pattern with the presenting movement disorder was a revealing diagnostic clue in all cases.

Suppressive effect of glucocorticoids on TNF-alpha production is associated with their clinical effect in multiple sclerosis.

A reduced sensitivity to glucocorticoids can affect the clinical effect of treatment with high-dose intravenous methylprednisolone in multiple sclerosis. We prospectively studied 27 multiple sclerosis patients who were treated with intravenous methylprednisolone. Before and after treatment in vitro stimulated TNF-alpha production in blood cells and the effect of in vitro administered glucocorticoids were determined as a measure of glucocorticoid sensitivity.

Outcome measurement in multiple sclerosis: detection of clinically relevant improvement.

Because the development of new treatments in multiple sclerosis as well as the awareness of the importance of patient-oriented measures have become more important in the last two decades, new outcome measures have been developed with the aim of being more responsive to change and more clinically relevant to patients. The ability to detect improvement is sparsely studied. In the present study we evaluate the responsiveness of the Expanded Disability Status Scale and two quantitative tests (the timed 25-foot walk test and the nine-hole peg test) separately and in combination, to detect improvement after intravenous methylprednisolone.

A glucocorticoid receptor gene haplotype (TthIII1/ER22/23EK/9beta) is associated with a more aggressive disease course in multiple sclerosis.

Context: In patients with multiple sclerosis (MS), glucocorticoids (GCs) might not be sufficiently able to restrain the immune system, possibly due to decreased GC sensitivity. This may be, at least partially, genetically determined. Previously, we reported a more aggressive disease course in patients with the glucocorticoid receptor (GR) gene ER22/23EK polymorphism, which has been shown to decrease GC sensitivity.

Whipple's disease in mentally retarded patients: report of two cases.

Of 21 patients diagnosed with Whipple's disease (WD) by polymerase chain reaction (PCR), 3 were mentally retarded. We describe 2 of these patients, both of whom had WD in the central nervous system. WD was confirmed with PCR on blood and, for 1 patient, also on cerebrospinal fluid (CSF).

Proteolytic shedding of the macrophage scavenger receptor CD163 in multiple sclerosis.

The scavenger receptor CD163 is selectively expressed on tissue macrophages and human monocytes. CD163 has been implicated to play a role in the clearance of hemoglobin and in the regulation of cytokine production by macrophages. Membrane CD163 can be cleaved by matrix metalloproteinases (MMP) resulting in soluble CD163 (sCD163).

The impact of glucocorticoid receptor gene polymorphisms on glucocorticoid sensitivity is outweighted in patients with multiple sclerosis.

Glucocorticoid (GC) sensitivity varies considerably in healthy controls as well as in patients with chronic inflammatory diseases like multiple sclerosis (MS). We investigated whether polymorphisms in the glucocorticoid receptor (N363S, ER22/23EK, and the BclI) were responsible for altered GC sensitivity. In healthy controls we found an association between the N363S allele of the GR and a reduced peripheral GC sensitivity.

Sensitivity to glucocorticoids is decreased in relapsing remitting multiple sclerosis.

Endogenous glucocorticoids (GC), which are under control of the hypothalamic-pituitary-adrenal axis, play an important role in controlling chronic inflammatory demyelinating diseases, like multiple sclerosis (MS). Increased hypothalamic-pituitary-adrenal axis activity has been found in MS patients and appeared to be negatively associated with acute inflammation. Exogenous GC are frequently used to treat relapses in MS, but the response to this treatment differs among patients, suggesting differences in sensitivity to GC.

No association of Fc gamma RIIa, Fc gamma RIIIa and Fc gamma RIIIb polymorphisms with MS.

Anti-myelin IgGs occur in the cerebrospinal fluid (CSF) and serum of multiple sclerosis (MS) patients, and can induce inflammatory effector functions in leukocytes by crosslinking IgG receptors (FcgammaR). The efficiency of FcgammaR-mediated inflammatory processes is affected by functional polymorphisms of three Fcgamma receptors (FcgammaRIIa, FcgammaRIIIa, FcgammaRIIIb). The relevance of FcgammaR polymorphisms in MS was evaluated by studying the distribution of FcgammaRIIa, FcgammaRIIIa and FcgammaRIIIb genotypes in 432 MS patients and 515 healthy controls.

CTLA-4 and CD28 gene polymorphisms in susceptibility, clinical course and progression of multiple sclerosis.

The balance between CD28 and CTLA-4 signalling is important for regulation of the immune response. We were interested whether a genetically mediated disturbance of this balance could be related to susceptibility or severity of multiple sclerosis (MS). We examined three polymorphisms in these genes, CTLA-4-318, CTLA-4+49 and CD28-I3+17, in 514 patients with MS and 181 controls.