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Transplantation of autologous chondrocytes obtained from cellular culture constitutes one of the methods of the biological treatment of the degenerative disc disease (DDD). The study covered a group of 50 patients operated on for single-level lumbar discopathy in whom material for autologous chondrocyte culture was sampled from a removed fragment of an intervertebral disc. The chondrocytes obtained from the culture were next implanted into the pre-operated space with the use of the percutaneous method, the implantation being followed by a radiological and clinical evaluation. In two cases a repeated prolapse of a nucleus pulposus fragment was reported after an earlier transplantation. The patients were operated on again. The material obtained from the recurred nucleus pulposus hernia allowed for a biological evaluation of the effect of the transplantation on the structure of the intervertebral disc with a light and confocal microscope. The examination showed good integration of the transplanted cells with the cellular matrix and their correct production activity in the form of the generation of typical matrix components – type I, II, III, IX collagen, proteoglycans and aggrecan as well as type IV collagen, atypical for the matrix, the presence of which is a subject of further research works.

Occipital neuralgia might have a various etiology but the most common cause is hypertrophic fibrosis of subcutaneous tissue following trauma to the occipital region, surrounding the occipital nerve. The other important cause of neuralgia is spondylosis of the upper part of the cervical spine (C1-C2). Rare causes are-diabetes, gout and neoplasm. In the presented material we point out the possibility of the occipital neuralgia after surgery in the treatment of the tumours of ponto-cerebellar region and trigeminal neuralgia. We observed the symptoms in two groups of patients and used pharmacological treatment, local blockade and cutting (neuronectomy) of the occipital nerves trunk when the conservative treatment was unsuccessful. We also present the present concepts of occipital neuralgia treatment. In case of severe symptoms, unsuccessful conservative therapy and poor results of the neuronectomy the most indicated therapy is selective posterior rhizotomy.

Brain tissue of rats pretreated with methylprednisolone or with the 21-aminosteroid U74389F, and that of untreated control rats, was assessed for the expression of Annexin-l (Anx-1) and the transcription of its mRNA. For this purpose Anx-1 cDNA was amplified and simultaneously a T7-RNA-polymerase promotor was incorporated into the cDNA using Polymerase Chain Reaction (PCR). Then digoxigenin-ll-UTP was incorporated into the transcribed cRNA with T7-RNA-polymerase. With this probe ill situ hybridization was carried out in sections of the brain. The probe was visualized by an immunoassay using an anti-digoxigenin antibody conjugate. Anx-1 protein was assessed by means of immunohistochemistry using a polyclonal antibody. The various brain areas of the control animals showed an appreciable amount of Anx-1 at mRNA or protein level; on the other hand, the animals which had been pretreated with either steroid, showed a more intense Anx-1 mRNA signal than the controls in many areas. In the pretreated animals Anx-1 immunostaining was unchanged in cortex, basal ganglia, amygdala and septum, but more intense in hippocampus, hypothalamus and thalamus. In ependyma, choroid plexus, meninges, and vascular walls there was no Anx-1 mRNA transcription detectable. An opposite profile was shown by the Anx-1 immunoreactivity, the protein was present in control animals as well as the steroid-pretreated animals, suggesting that here the protein was either from systemic origin, or has diffused from adjacent structures. The results indicate that Anx-1 mRNA transcription is upregulated by either steroid, and that in the untreated animals there is a resting level of Anx-1 mRNA transcription, presumably reflecting physiological influences on Anx-1 expression.

Using in vivo proton-magnetic resonance spectroscopy (H-1-MRS), which allows the measurement of metabolites of adequate tissue concentration, the origin of lactate in peritumoral edema has been assessed by comparison with lactate levels in the central and marginal areas of the tumor in 18 patients with cerebral gliomas. In the majority of cases lactate content in the area of peritumoral edema was lower than that in the tumor margin or tumor center, which is consistent with the assumption that the tumor is the source of lactate, which then reaches the surrounding area of edema by diffusion. In 3 of the 18 cases the amount of lactate in the peritumoral edematous tissue was higher than in the tumor, indicating that the lactate is locally produced on account of ischemia due to regional elevation of tissue pressure in the edematous area.