Experimental allergic encephalomyelitis (EAE) was studied in guinea pigs with an inherited deficiency of the fourth component of complement (C4) and in guinea pigs injected with cobra venom factor to deplete the third component and late-acting components of complement. EAE was elicited by immunization with homologous spinal cord or purified basic protein. Administration of cobra factor after the injection of encephalitogenic emulsion delayed the onset and reduced the intensity of the clinical manifestations of EAE. In addition, cobra factor markedly reduced mortality during the sixty days of observation. However, pathological changes of perivascular infiltration and demyelination were similar in cobra factor-treated and untreated animals. Clinical signs of EAE an mortality in C4-deficient guinea pigs were no different from those in normocomplementemic controls. Thus, although activation of the classic complement pathway does not appear to be involved in the production of EAE in guinea pigs, our results suggest a possible role of the alternative complement pathway in the pathogenesis of EAE.

In the period 1968 through 1977, multiple sclerosis (MS) was diagnosed in 349 patients at the Henry Ford Hospital. Of these, 312 were accepted in the study and 53 were blacks. In this medical center where the overall population consists of approximately 50 % blacks, the MS blacks comprised only 17 % of the total MS population. White and black MS patients did not differ significantly for clinical characteristics of MS or for death rates. The MS black patients were divided in two groups, Northernand Southern-born. The mean age of migration was 11.9 years. Southernborn blacks lived an average of 20 years in the North before the symptoms of MS began. Northem-born MS patients had a 5.5 earlier age of onset and the diagnosis was made 9 years sooner when compared with the Southern-born MS blacks. The Southern-born MS group more often showed a chronic progressive course wither initially or following a few exacerbations and remissions. These findings suggest that a possible genetic predisposition, as well as a geographically determined exposure to an environmental agent, may be related not only to the risk of developing MS, but in the American blacks may also influence the age of onset, the age of diagnosis, and even the clinical course of MS.

The first clinical case of transient traumatic locked-in syndrome is presented. The locked-in state lasted for 3 months. The patient’s neurologic deficit and the abnormal auditory evoked responses pointed to a lesion involving the left pons and ventral midbrain. The locked-in syndrome caused by a traumatic damage of the brain stem structures can be transient and thus it may have a better prognosis than the locked-in syndrome secondary to the occlusion of the basilar artery.

In three patients who fulfilled the clinical criteria of progressive supranuclear palsy, radiologic investigations suggested normal-pressure hydrocephalus. Shunt procedures in all three resulted in temporary improvement of gait, mentation, and bladder control, but gaze paralysis and extrapyramidal findings did not change.