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Abstract. Patients with a hereditary myopathy with paroxysmal myoglobinuria were studied in the chronic state of the disease. They were characterized by muscle contractions of fairly normal strength and quite good endurance in exercise with small muscle groups, but a poor physical performance in exercise of some duration with large muscle groups. Several facts indicate that it was not muscular weakness, but the circulatory capacity that was a main factor limiting the physical working capacity in exercise of some duration with large muscle groups. The oxygen uptake was largely normal in relation to the work performed. However, even light exercise on a bicycle ergometer caused tachycardia (approaching maximum heart rate), a high cardiac output (approaching, for the size of the individual, maximum values in the normal range) and an abundant blood flow through the exercising legs. Thus, there were no signs of insufficient heart function, but the utilization of the oxygen of the blood in the exercising limbs was low. The concentration of lactate, and particularly of pyruvate, in the blood, and the lactate and pyruvate production increased more than in the controls for the slight work performed. During exercise the lactate/pyruvate ratio decreased and the calculated “excess of lactate” was negative, while it increased in normal subjects. After exercise the excess lactate was higher in the patients than in the controls. This indicates an abnormal muscle metabolism, probably a decreased capacity for pyruvate oxidation. It is suggested that a metabolic disturbance caused an abnormally large production of metabolites in the working muscles, resulting in muscular vessel dilatation by a local humoral effect. The muscles acted almost like a‐v shunts and, as a consequence, the patients had a hyperkinetic circulation, i.e. a low O2 uptake in relation to cardiac output, a low a‐v O2 difference for mixed venous blood and for the venous blood of the exercising limbs.

Cerebrospinal fluid (CSF) samples obtained by consecutive lumbar puncture of 26 patients with presumed pale cerebral infarction, 66 with presumed hemorrhagic infarction, 16 with lobar hematoma, and 18 with cerebral infarction verified at autopsy, were examined with a cytological method permitting a total and differential cell count. A transitory outflow of polymorphonuclear neutrophilic leukocytes (PNL) was found in 70% of the patients with hemorrhagic infarction and lobar hematoma, with a peak three to four days after onset. The strongest PNL reaction was recorded in CSF from patients with lobar hematoma. In 75% of patients with pale infarction, no PNL or only a few PNL were found. In the autopsy group the PNL reaction in the brain as well as in the CSF was stronger in patients with hemorrhagic infarcts than in those with pale infarcts. (26:489-501, 1972) Key Words.\p=m-\Cerebrospinalfluid cytology; differential diagnosis of stroke; brain infarction; lobar hematoma; cerebrospinal fluid in cerebro-$ vascular disease.

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