I MEDIrCAL JOU3NA& denied until 1871, when C. E. Brown-Sequard, on experimenital grounds, argued that lesions of the pons caused haemorrhages, and injuries of the medulla oblongata oedema of the bases of the lungs as a result of impulses transmitted through branches of the sympathetic 'eaving the cord in the uplper dorsal region. Rose Bradford anid Dean (1889, 1S94) founid that in the dog vasomotor nerve fibres derived from the upper (loirsal nerve supply the pulmonary blood vessels, though the

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... pulmonary vasomotor mechanism is poolrly developed as compared with that regulating the systemic arteries. They also conckl(led that the pulmonary circulation is comparatively independent of the systemic, and that alterations in tIme blood pressure of the latter must be so considerable asto interfere with the action of the cardiac valves andl l)produce regurgitation before affecting the pulmonary blood pressure. On the other haInd, Brodie and Dixon, in 1904, denied thle vasomotor control-of the )ulmonary circulation, anid in 1928 Dixon aind Hoyle conifirmed this. In the nmeanwhile Fuihner and Starling, using the heart-lung plreparation, founid a considerable degree of pulmonary vaso-constriction and a rise of pulmonary arterial pressutre with adrenaline, and in 1905 Fran9ois-Franck came to a similar decision. In a critical review of the extensive work on thle subject Wiggers, in 1921, concluded that reflex vasomotor effects on the pulmonary circulation must be regarded as probable rather than proved. -The intracranidl cirevlation is re-markable for the rigid cranial cavity and -the water-bed o-f the cerebro-spinal fluid. Whether or not the nerves-Accompanying the cerebral vessels exert a vasomotor function hias been repeatedly investigated, but with discordant results; Roy and Sherrington (1890), L. Hill (1896), and niore rlecently Florey (1925) who found that the cerebral artenies and the cerebral ends of the capillaries rleact to mechlanical, thermal, electrical, and chemical stimuli bv cointractioni and dilatation, agree that there is not any evidence of nervous control over the cer:ebral vessels. On the other hand, the existence of active futnctional control of the cerebral vessels by vasomotor nerves has been supported by Claude Bernard (1858), Nothnagel (1867), Wiggers (1915), Forbes and Wolff (1928), and others. The exp}erimental observations are of imluch interest in connexion with the belief held by many clinicians that transient paralyses, such as occur without evidence of a gross lesion, mav be due to spasm of the cerebral arteries analogous to that in Raynaud's disease. Osler (1ml1), in describing transient attacks of aphasia and paralvsis in states of high blood pressure and arterio-sclerosis, accepted the view put forwar-d by Peabody (1891) , W. Russell (1909), and others that they were due to transient spasm. -Florey has thrown out the suggestion that possibly in pathological conditions, such as arteriosclerosis, an abnormnial metabolic product which has not any effect on normal blood vessels may produce spasm of damaged arlteries. The influence of the conditions of the cerebral circulation on the general blood pressure has beeni much discussed. Starling and Anrep (1925) showed that when imperfectly supplied with blood the vasomotor centre brings about a compen-satory rise of blood pressure, thus conifirming Cushing's earlier demonstration in 1901 that the vasomotor centre exerts a regulating influence whereby anaemiia of the medulla oblongata is prevented when the intracranial pressure is increased-above that in the cerebral vessels. This was supported by Bordley and Baker's (1926) observation that in arterio-sclerosis a high blood pressuire was definitely associated with sclerosis of the arterioles of the medulla; this, however, was contested by Keith, Wagener, aind Kernolhain, and Cutler's observations showed that gross vascular changes in thje blood supply to the medulla were not responsible for blood pressuire chaniges. Experimentally Florey, Marvin, and Drurly (1928) found that lowering the blood pressure in the circle of Willis has not any influience uponl the general blood pressuive. ON RECOVERY FROM SY3MPTOMS OF INTRACRANIAL TUMIOUR. THAT an intracrall-ial tumour can exist without distinctive symptoms, and ev-en without suggestive symptoms, is a proposition that has for its warrant the suire teachiing of experience. Again, it is well recognized that even wlhen symptoms of tumour are present ther-e is often, in the cour'se of one and the same case, a wide varliation in the' degree of their severity, and, indeed, a period of quiescence may be so prolonged anid so pronounced as to cast suspicion on the accuracy of the diagnosis. Tile explanation of such experiences is tha-t for tile most part the sv-miptomns associated with intracranial tumour are due less to the mass of the tumour than to circulatory disturbances (congestions, anaemias, oedemas, haemorrhages, softenings) liable to occur in its neighbourhood, and to interferences wlhich thie tumour may exercise on the circulation of tlhe cerebr-ospinal fluid. Grant the absence of these accidents, and cerebral events and symptoms, in spite of the presence of a tumour, may be slight, non-suggestive, and ev-en nonexistent.* With these positions admitted, mav it not be possible that symptoms, and even pronounced symptoms, of intracranial tumour may disappear, not merely for a more or less brief period, but completely and perlillanently? For if in an individual case the intracranial accidents or complications, and the symptoms which result fromii these, may after a period of activity subside, the possibility that such quiescence may be l)ermanent can at least be contemplated. Assume that the tumour ceases to grow or perhaps shrinks .in size, anid. that in this or i1i some other faslhion it no longer causes the intracranial disturbances on which the * A recent example is reported by Professor Sydney Smith, Britis7e Medi6al Journal, January 22nd, 1927. clinical evidences of tumour mainly depend, and it is no violent l)rol)osai to suiggest the possibilitv of a clinlical recoi d in wliich the symptoms of intracraniai tuimour disapp ear completely and tlhe paleient regains a level-of good health. The clinical hiistory, iinfortunately, inarchets usuallh in the opposite direction, but there is nothing in the natuie of things to renider exceptions to this rule impossible, aiid the principal object of this communication is to suggest that such exceptions do actuallv occUr1 This suggestion has for its support case records (adm-ittedly excel)tional) marked in the earlier stage by symptoms-regarded as conclusive of intracranial ttimour, while-latbr thlese symptoms disappear and the patient sueceeds to good liealth. Such experiences, of coulrse, call for an explanation, and the explanation here proposed is cessation of initracranial, disturbances coiisequent on quieseence or shrinkiiig of the tumour growth. That recovery from symptoms of intracranial tumour, except for blinidness due to optic atro)hy, actually occurs there can be no doubt. Records of patients who in earlier vears hav-e suffer-ed a severe illnless-ch<aratterized by headache, vomitinlg, anid optic neuritis, and who, but for loss of sight, have later nmade a good recovery, are well established. It may be suggested that these cases are not cases of tumtnouir, and it mlust be admitted that in exceptional instances the symptoms -just quoted have existed and yet ino tumnour has beeni found on post-mrlortem examination;l sutch coniditions as hydrocephalws,2 serous meningitis,3 or sinus thiombosis4 may-perhapsbe advanoed as alternati-es to tunmour. On the otlher hand, in many patients who are blind from optic atropliy after an illness distinguislhed by cerebral symptoms, competent clinical observers plresent at the time of the original illness have felt no doubt that the symptoms meant intracranial tumour; and nlow and again in the brainof a patient included in tills group, and dying years after the primary illness, a tu-miour lhas been p)resent to post-ortlem demonstration. Thus it is certain that within the natural .history of intracranial tumours room must be found for cases in which all active evidences of the presence of u tumour disappear, the former cerebral disturbances being