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An experimental investigation was performed to examine the influence of ACTH on the long-term results of muscle regeneration after nerve repair. Twenty albino-rabbits ("White Russians") served as the animal model. The epi-perineural neurorrhaphy of the fibular nerve was carried out under microscopic control with 11x0 sutures. A computer-supported light-microscopic analysis of representative muscle-fiber diameters was performed for detection of nerve regeneration on the effector muscle of the peroneal nerve, the anterior tibial muscle, after 3, 4, 5 1/2, 7, and 8 months. In addition, the nerves were examined by light microscopy using not only standard techniques but also surgical immunohistological staining techniques (APAAP). The acceleration of nerve regeneration already described in the literature was confirmed by our investigations. However, the results observed after eight months were similar, regardless of the ACTH dosage applied. Muscle regeneration was not influenced by the injection of ACTH. It therefore does not appear justifiable to clinically apply ACTH for improvement of nerve and muscle regeneration.

This study quantifies the neurological structures of the ACL from proximal to distal in the zones A, B and C. 37 knee cadavers of healthy patients were analyzed to determinate the innervation for each age decade. This investigation was undertaken with high specific immuno-histologic sections (APAAP method). Neurofilaments and Schwann cells were isolated identified. In a second group consisting of 15 patients with idiopathic arthritis the ACLs were analyzed. This showed a significant loss of innervation, often, there was a complete deficit. In conclusion, this study revealed that idiopathic arthritis of the knee is associated with a significant deficit of the innervation of the ACL. If this is the reason for the arthritis or a secondary phenomenon is still unknown.

In this survey article on Borna Disease-many years after the review of Zwick (1939)-again a modern comprehensive summary of "Borna Disease virus infection" is given. The infection occurs in horses and sheep, furthermore, in laboratory animal species inoculated experimentally; its clinical, virological and neuropathological features have been described in numerous presentations. Clinical symptoms in naturally and experimentally infected animals are characterized by initial alterations in the sensorium. The neurological symptomatology of the disease (disturbances in coordination, motor, sensory and vegetative symptoms) reflect the presumed localisation of the virus in various brain areas and the course of the disease supports the assumption of intraneural spread of the agent. In horses the incidence is highest during spring. Experimental infections show an exceptionally broad spectrum of infectible animals extending from higher mammals to birds. Our investigations make it clear that we have to differentiate between infections followed by disease (e.g. horse, rabbit, older rat) and persistent infections without overt clinical symptoms (mouse, chicken). Persistent infections are sometimes associated with fine alterations in behaviour (tree shrew) or decreased learning ability (mice). Borna Disease virus, which has not been characterized up to now, is known to grow without any cytopathic effect in tissue cultures. All tested cell lines (including those from man) could be infected. The investigations indicate that Borna Disease virus comprises an enveloped RNS-containing agent. The infection induces the production of specific antigens such as a complex known as the soluble antigen, and a 14500 dalton protein. Under natural conditions and in experimentally infected animals antibodies are produced against such soluble proteins and determinants involved in neutralization of the virus. In the central nervous system (CNS) a local immune response accompanied by the production of oligoclonal immunoglobulins is demonstrable. Besides the humoral reaction it was possible to study the influence of cellular defence mechanisms on the disease process in monkeys, rats and rabbits. Histopathologically, Borna Disease is characterized by a non-purulent inflammation of the brain and the spinal cord. Most alterations are found in the grey matter, mainly in the Ammon's horn, olfactory lobe, caudate nucleus, thalamus, lamina quadrigemina and in he cerebellar nuclei. The perivascular infiltrations, consisting of lymphocytes, histiocytes and plasma cells are most conspicuous. Occasionally, degenerative alterations are observed in ganglion cells.(ABSTRACT TRUNCATED AT 400 WORDS)

The neuropathological findings in 13 patients with the acquired immune deficiency syndrome (AIDS) and with AIDS related complex (ARC) are reported. Six patients presented with neurological symptoms, whereas autopsy revealed CNS involvement in nine cases. Four patients showed neither neurological nor neuropathological abnormalities. The most frequent neuropathological diagnoses were toxoplasma encephalitis (4 cases) and multiple or solitary cerebral necroses (3 cases). Long tract degeneration of the spinal cord was found in 2 cases. Cytomegalovirus infection, progressive multifocal leukoencephalopathy, primary lymphoma of the CNS, infiltration of the leptomeninges by plasmocytoma cells and a solitary metastasis of a bronchial carcinoma were diagnosed in one case each. Subacute leukoencephalitis, mentioned frequently in the literature, was not present in this material. In one case, however, status spongiosus and gliosis was found in the cortex and basal ganglia. As similar spongy changes can be seen in mice infected experimentally with retroviruses, a pathogenetic role of the human T-cell lymphotropic/leukaemia virus type III (HTLV-III) cannot be ruled out. Astrogliosis and hypertrophy of astrocytes were found in nine cases. Morphometrically, the number of astrocytes was significantly higher in AIDS patients than in control cases which were selected randomly on grounds of comparable age. Whether this finding bears some relationship with HTLV-III encephalopathy remains open to further investigation. Glial nodules were found in four cases; according to silver impregnation they were composed of microglial elements.

Certain neurotropic viruses are carried along neuronal processes by the axonal transport mechanisms. Indirect morphologic evidence suggests that viral nucleic acid can be transmitted to other neurons by transsynaptic passage. Through this mechanism the viral genome can reach widespread and remote brain areas by propagation along neuronal networks in an intracellular milieu. This type of propagation does not require completion of full replication cycles for cell-to-cell spread; transmission of infective viral nucleic acid is in itself sufficient.