We have identified a cell type in 7-day-old rat optic nerve that differentiates into a fibrous astrocyte if cultured in the presence of fetal calf serum and into an oligodendrocyte if cultured in the absence of serum. In certain culture conditions some of these cells acquire a mixed phenotype, displaying properties of both astrocytes and oligodendrocytes. These observations suggest that fibrous astrocytes and oligodendrocytes develop from a common progenitor cell and provide a striking example of developmental plasticity and environmental influence in the differentiation of CNS glial cells.

A glial progenitor cell that develops in vitro into an astrocyte or an oligodendrocyte depending on culture medium

This is a proposal of the Movement Disorder Society for a clinical classification of tremors. The classification is based on the distinction between rest, postural, simple kinetic, and intention tremor (tremor during target-directed movements). Additional data from a medical history and the results of a neurologic examination can be combined into one of the following clinical syndromes defined in this statement: enhanced physiologic tremor, classical essential tremor (ET), primary orthostatic tremor, task- and position-specific tremors, dystonic tremor, tremor in Parkinson's disease (PD), cerebellar tremor, Holmes' tremor, palatal tremor, drug-induced and toxic tremor, tremor in peripheral neuropathies, or psychogenic tremor. Conditions such as asterixis, epilepsia partialis continua, clonus, and rhythmic myoclonus can be misinterpreted as tremor. The features distinguishing these conditions from tremor are described. Controversial issues are outlined in a comment section for each item and thus reflect the open questions that at present cannot be answered on a scientific basis. We hope that this statement provides a basis for better communication among clinicians working in the field and stimulates tremor research.

Consensus statement of the Movement Disorder Society on tremor

L'incidence annuelle du syndrome de Guillain-Barre est de 1,5/100000 habitants La mortalite actuelle est estimee a environ 5 % d'apres des essais therapeutiques recents, bien conduits Dix pour cent des malades gardent des sequelles motrices tres invalidantes un an apres le debut des premiers signes neurologiques La prise en charge de ces malades necessite des equipes entrainees, multidisciplinaires, pouvant pratiquer l'ensemble des therapeutiques specifiques La corticotherapie per os'ou par voie intraveineuse est inefficace Les echanges plasmatiques sont le premier traitement dont l'efficacite a ete demontree par rapport a un groupe controle Les indications sont maintenant mieux connues Les formes benignes (marche possible) beneficient de 2 echanges plasmatiques; 2 echanges supplementaires sont realises en cas d'aggravation Dans les formes intermediaires (marche impossible) et les formes severes (recours a la ventilation mecanique), 4 echanges plasmatiques sont conseilles Il n'est pas utile d'augmenter leur nombre dans les formes severes ou en cas d'absence d'amelioration De fortes doses d'immunoglobulines donnees par voie intraveineuse (lq IV) [0,4 g/kg/j pendant 5 jours] sont aussi efficaces que les echanges plasmatiques dans les formes intermediaires et severes Dans ces formes, le choix entre Ig IV et echanges plasmatiques depend des contre-indications respectives de ces traitements et de leur faisabilite Les travaux en cours ont comme objectif de mieux preciser les indications respectives des echanges plasmatiques et des lq IV dans des formes de gravite differente, leur morbidite comparee, la dose optimale des lq IV

[Guillain-Barré syndrome].

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(06)68175-0.pdf

Guillain-Barré syndrome

Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the p...

/pdf/biology-of-oligodendrocyte-and-myelin-in-the-mammalian-3ggbjcby4w.pdf

Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

THE increasing use of tissue culture techniques in neurobiological studies has created an urgent need for cell-type specific markers which would allow unambiguous identification of the different types of neural cells. We show here that galactocerebroside (GC), the major glycolipid in myelin1, can serve as such a cell-surface marker for cultured rat oligodendrocytes, the glial cells responsible for making myelin in the central nervous system.

Galactocerebroside is a specific cell-surface antigenic marker for oligodendrocytes in culture

Background Although infection with Campylobacter jejuni is recognized as a common antecedent of the Guillain–Barre syndrome, the clinical and epidemiologic features of this association are not well understood. Methods We performed a prospective case–control study in a cohort of patients with Guillain–Barre syndrome (96 patients) or Miller Fisher syndrome (7 patients) who were admitted to hospitals throughout England and Wales between November 1992 and April 1994. Bacteriologic and serologic techniques were used to diagnose preceding C. jejuni infection. Results There was evidence of recent C. jejuni infection in 26 percent of the patients with Guillain–Barre or Miller Fisher syndrome, as compared with 2 percent of household controls and 1 percent of age-matched hospital controls (P<0.001). Of the 27 patients with C. jejuni infection, 19 (70 percent) reported having had a diarrheal illness within 12 weeks before the onset of the neurologic illness. No specific serotypes were associated with Guillain–Barre ...

https://www.nejm.org/doi/pdf/10.1056/NEJM199511233332102

Campylobacter jejuni infection and Guillain-Barré syndrome.

Pathogenesis of Guillain-Barré syndrome.

Campylobacter jejuni, a Gram-negative spiral bacterium, is the most common bacterial cause of acute human gastroenteritis and is increasingly recognized for its association with the serious post-infection neurological complications of the Miller-Fisher and Guillain-Barre syndromes. C. jejuni lipopolysaccharide (LPS) is thought to be involved in the pathogenesis of both uncomplicated infection and more serious sequelae, yet the LPS remains poorly characterized. Current studies on C. jejuni suggest that all strains produce lipooligosaccharide (LOS), with about one-third of strains also producing high-molecular-weight LPS (referred to as O-antigen). In this report, we demonstrate the presence of the high-molecular-weight LPS in all C. jejuni strains tested. Furthermore, we show that this LPS is biochemically and genetically unrelated to LOS and is similar to group II and group III capsular polysaccharides. All tested kpsM, kpsS and kpsC mutants of C. jejuni lost the ability to produce O-antigen. Moreover, this correlated with serotype changes. We demonstrate for the first time that the previously described O-antigen of C. jejuni is a capsular polysaccharide and a common component of the thermostable antigen used for serotyping of C. jejuni.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2958.2000.01717.x

Genetic and biochemical evidence of a Campylobacter jejuni capsular polysaccharide that accounts for Penner serotype specificity

To clarify the association between Campylobacter jejunei (Cj) infection and antibodies to ganglioside GM1 (anti-GM1) in Guillain-Barre syndrome (GBS), we have carried out a prospective case-control study of 96 patients with GBS. Cj infection occurred in 25 (26%) patients. IgG and/or IgM anti-GM1 were identified in 24 (25%) patients and in 1 of 71 (1.4%) household controls (p < 0.001). Thirteen of the 25 (52%) Cj-postive patients had anti-GM1 compared with 11 of the 71 (15%) Cj-negative patients (p < 0.001). Neither the peak overall disability nor the 1-year disability differed between the anti-GM1-positive and anti-GM1-negative patients. However, patients with the combimation of Cj infection and anti-GM1 positivity recovered more slowly than Cj/anti-GM1-negative patients (p = 0.05), were more likely to have axonal degeneration, and were significantly more disabled at the end of 1 year (p = 0.02). The presence of Cj infection is more important than anti-GM1 postivity in determining the extent of axonal involvement and, hence, prognosis. Since the presence of anti-GM1 is not a significant poor-prognostic factor, a search should be made for other properties of Cj infection that would account for its relationship to axonal degeneration.

Norman A. Gregson

Papers

Galactocerebroside is a specific cell-surface antigenic marker for oligodendrocytes in culture

Campylobacter jejuni infection and Guillain-Barré syndrome.

Pathogenesis of Guillain-Barré syndrome.

Genetic and biochemical evidence of a Campylobacter jejuni capsular polysaccharide that accounts for Penner serotype specificity

Anti‐ganglioside GM1 antibodies in guillain‐barré syndrome and their relationship to Campylobacter jejuni infection