Spinal cord sarcoidosis

We present a case of spinal cord sarcoidosis which resembled a disseminated intramedullary tumour. The case is unusual because the spinal cord is only rarely affected by sarcoidosis and the patient developed a neurological deficit as the first manifestation of the disease. This condition thus has to be considered in the differential diagnosis of primary intramedullary tumours, or metastatic disease with involvement of the spinal cord.     

Bilateral facial palsy: Epstein–Barr virus, not Lyme disease

Bilateral facial palsy is frequently linked with lyme disease. We report a patient with bilateral facial palsy due to Epstein-Barr virus infection but with Borrelia burgdorferi IgM in serum caused by polyclonal B-lymphocyte stimulation.     

Abnormal astrocyte differentiation and defective cellular interactions in wobbler mouse spinal cord

Summary The wobbler mutation is inherited as an autosomal recessive trait and displays a muscular atrophy associated with motoneuron degeneration in early postnatal development. It has been shown that the level of glial fibrillary acidic protein (GFAP) is greatly increased in the spinal cord of wobbler mice. We performed immunocytochemical analyses combined with confocal microscopy to study the developmental distribution of GFAP-positive astrocytes in the spinal cord of wobbler mice during the course of the disease, and in primary cultures of adult wobbler spinal cord astrocytes. Many changes in the number and distribution of astrocytes were observed in the wobbler mice from 1–10 months post-partum. Strongly GFAP-positive astrocytes are present in small number in the anterior horn by 1 month. They increase in number and are observed in the entire spinal cord grey and white matters by 2–10 months. These reactive astrocytes have thick, short, extensively branched processes which contrast with the long, unbranched processes observed in control mice. The wobbler astrocyte processes are oriented perpendicular to the surface of the spinal cord, which contrasts with the normal parallel, concentric orientation. No expansion of astrocyte processes exit from the white matter towards the grey matter. Moreover, the surface of the wobbler spinal cord beneath the meninges displays a dramatic decrease of interdigitating processes, end feet and flattened cell bodies of astrocytes that form a disorganized layer.In vitro, mutant astrocytes have morphological characteristics similar to thosein vivo and, in particular, develop short, thick, branched processes. These mutant astrocytes in cultures do not contact one another, whereas normal mature cultures show an increased incidence of cell-cell contacts between long processes. The increase of astrocyte reactivity associated with these modifications in astrocytic process arrangement may reflect an important primary event in the course of the wobbler disease rather than a non-specific response to motoneuronal death.