[Hypermetabolism in head injury and tetanus: patho-physiological and new therapeutic conceptions]

Longlasting overactivity of the sympathetic nervous system can be considered as one of the causes of the hypermetabolism developing in patients with head injury or tetanus. In tetanus elevated plasma levels of catecholamines can be demonstrated as long as disturbances of the motor nervous system are present. In patients with head injury the plasma catecholamines, mainly noradrenaline, start to increase with the onset of the transition stage from midbrain syndrome to the apallic syndrome. The activity of the sympathetic nervous system remains elevated also in the full stage of the apallic syndrome and during the remission. The influence of such a longlasting sympathetic overactivity on the metabolism is discussed. For the suppression of hypermetabolism caused by sympathetic overactivity the use of the adrenergic neuron blocking drug debrisoquine combined with a nonselective beta-adrenergic blocking drug is suggested. This treatment enables a normocaloric nutrition in patients with head injury or tetanus. Additionally such a treatment protects the cardiovascular system against the consequences of a longlasting sympathetic overactivity. The influence of debrisoquine on the plasma levels of noradrenaline is demonstrated in a patient with head injury.