Immune-mediated ataxias are common. Advances in genetic testing have significantly improved the diagnostic yield of patients suspected of having a genetic ataxia. Making a diagnosis of the cause of ataxia is essential due to potential therapeutic interventions for immune and some genetic ataxias.

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Hemorrhage experiments both of an acute and chronic type were carried out in dogs. The adrenal vein was cannulated as in the previous experiments. There were 10 dogs studied during acute hemorrhage and 4 dogs in chronic hemorrhage. Blood loss in these animals produced an immediate and marked increase in concentration of the catechol amines in the adrenal vein blood, this increase being in proportion to the fraction of the total blood volume removed. The increase was due primarily and initially to an increase in concentration of epinephrine rather than norepinephrine in the adrenal venous blood. The maximum output of catechol amines occurred at a variable time and was then followed by a gradual decline. Early retransfusion of the lost blood or replacement by blood substitute immediately and drastically reduced the catechol amine output. The peripheral arterial blood concentrations of epinephrine were higher than the venous blood concentrations and appeared to be more closely correlated with the concentrations in adrenal venous blood. Infusions of norepinephrine in two dogs increased the output of epinephrine and norepinenephrine in the adrenal vein blood. There was no sign of adrenal medullary failure in dogs dying from shock due to blood loss, even when these dogs accepted blood from an upbleeding (Lamson) bottle by ‘taking up.’

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