Five experimental methods were employed in dogs, to analyse the transmission of encephalic stimuli to the heart by either neural or circulatory pathways. 1. Cerebral-cardiac cross-circulation in parabiotic dogs. 2. Interruption of all nervous connections by bilateral vagotomy and cross-section of the cervical spinal cord. 3. Pharmacological blocking of the sympathetic and parasympathetic nervous system by dihydroergotamine and atropine, in combination with mid-cervical section of the vagus nerves. 4. Depletion of tissue catecholamine supplies by reserpine. 5. Blockade of autonomic ganglia by hexamethonium. These experiments proved the exclusive importance of nervous pathways for the transmission of encephalic stimuli to the heart. In animals with crossed cardiocerebral circulation, cerebral compression produced electrocardiographic changes only in the isolateral dog, but not in the parabiotic dog whose heart received all the venous outflow from the contralateral injured brain. After cervico-medullar section plus vagotomy, cerebral compression had no effect on the heart anymore. Pharmacological blocking, by atropine, dihydroergotamine, and vagotomy did not prevent electrocardiographic disturbances after brain injury. The importance of vagal pathways is herewith excluded. The failure of dihydroergotamine, to inhibit the cardiac effect of cranial injury might be explained by an insufficient neutralization of endogenous adrenaline and nor-adrenaline. The pathogenic importance of these substances is also suggested by the abolition of encephalogenic heart lesions after reserpine treatment. Paradoxically, high doses of hexamethonium that completely block parasympathetic ganglia do not hinder, in acute intracranial hypertension, either the pronounced rise of arterial blood pressure nor the appearance of typical encephalogenic heart lesions.