A 13-year-old boy developed closely spaced episodes of recurrent febrile meningitis that persisted for 22 months despite antibiotic therapy. During exacerbations the cerebrospinal fluid contained up to 2,500 leukocytes per cubic millimeter, including up to 20% activated monocytoid cells, with high IgM and IgG levels. No cause for the disorder was found, but steroids improved the condition and colchicine therapy apparently cured it.

SUMMARY We determined the respiration, respiratory control, and Pi:O ratios with different substrates in mitochondria isolated from five cases of human neuromuscular disorders (two cases of central core disease, two cases of neuropathy of Dejerine-Sottas, and one case of KugelbergWelander's disease) and compared them with normal human muscle. In all the myopathies studied, a severe derangement of the respiratory control with variable derangement of oxidative phosphorylation was found. This supports the idea that a group of neuromyopathies shares the same biochemical lesion as the so-called mitochondrial myopathies, forming with them a group of myopathies which may be related through a similar biochemical lesion of varying degree. Alternatively, disturbance of mitochondrial functions in a number of myopathies could be considered as a non-specific finding.Despite the frequent occurrence of morphological changes in mitochondria in many types of human neuromuscular disorders (Gruner, 1963;Aleu and Afifi, 1964;Gonatas, Perez, Shy, and Evangelista, 1965;Norris and Panner, 1966;Gonatas, 1967;Engel and Dale, 1968;Chou, 1969), several myopathies have been described in which abnormalities of this organelle were -considered to be of major significance (Luft,

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Fifteen patients with subacute sclerosing panencephalitis in different evolutive phases were studied with clinical and electroencephalographical methods, and the data obtained were compared with the data obtained by electrophoretic an immunochemical methods. The electro‐phoretic examination of CSF proteins was carried out on a support of cellulose acetate and evaluated by comparison with a “control” group comprising 100 subjects. It is observed that panencephalitis tends to evolve in two distinct phases. The first phase usually ranges up to the first six months of evolution and presents a clinical picture of dementia, myoclonus, and characteristic periodical complexes in the EEG. In this phase the values for total CSF proteins are normal, with selective hypergammaglobulinorrachia and decrease of almost all other electrophoretic fractions. In the second phase, with evolution periods of more than six months, the clinical picture is that of decortication, with low voltage of the EEG. In this phase the total CSF proteins are increased. The gammaglobulin increase is great, but there is also an increase of the remaining electrophoretic fractions. Authors ascribe these alterations to changes in the blood‐brain barrier during the evolutive course of the disease.