Pulmonary Oedema and Intracranial Lesions

JOURNAL~~~~~Two skulls were also cracked through lack of precautions.Now there is evidence that non-traumatic risks are present which if numerically fewer are no less unpleasant or hazardous.Summary The foregoing occurrence of acute pulmonary oedema with neurological disturbance followed promptly after completing the " mess trick " and the "fainting lark."Syncope in each case occurs through well-established physiological vascular changes.Lung trauma is considered to be an improbable cause of pulmonary oedema.Neither cerebral thrombosis nor cerebral haemorrhage is thought to be likely as a cause of neurological disturbance.A proved connexion exists between pulmonary oedema and cerebral damage: both conditions have been confirmed at post-mortem examination.With lesser degrees of cerebral damage recovery from pulmonary oedema may occur.The infliction of discrete lesions to the hypothalamic pre-optic nuclei in experimental animals is regularly followed by acute and severe pulmonary oedema.Un- inhibited vasomotor impulses in these animals will move blood from regions of high contrictor potential into lung vessels possessing low constrictor potential.The pulmonary oedema that follows is essentially neuro-haemodynamic in origin.By applying to man the principle elicited by this experimental work, an unusual symptom-complex after the fainting lark or mess trick becomes understandable.The presence is postulated, in these people, of unsuspected anatomical and morphological anomalies in the ultimate arterial supply to the hypothalamus and upper brain-stem; this, coupled with the very marked reduction in overall cerebral blood flow that accompanies a dedicated per- formance of the fainting lark, is calculated to deprive of blood both the oedemagenic centre in the hypothalamus (presumed to exist in man) and parts of the upper brain- stem.It would be tantamount to their sustaining arterial shutdown.Therefore this reversible neural disturbance most probably causes neuro-haemodynamic changes which result in pulmonary oedema and a variable neural dysfunction in the upper brain-stem. I am indebted to the