Up to a certain point the vaso-motor centre holds the whip-hand. The capillary anæmia as produced by the compression force—cerebro-spinal tension, &c.—brings about a condition which not only acts as a stimulus to the vaso-motor centre but also exercises a marked effect on the vagus and respiratory centres. The blood-pressure rises, the pulse is slowed in rate, and its tension markedly increased, whilst the respiration is slightly irregular both in depth and rhythm. The vaso-motor centre thus attacked sends out further impulses so as to raise the blood-pressure to slightly above requirements. The bulbar centres are again flushed with blood, the vaso-motor centre ‘slacks off’, and the blood-pressure falls again.
The compressing force is, however, still active and full of fight. A further capillary anæmia results. The vaso-motor centre again responds and the blood-pressure rises higher than ever, the pulse-rate is further slowed, and the respiration is deeper, less regular, and even stertorous.
This combat continues, and, in the presence of an active compression force, there is that rhythmic activity of the vaso-motor centre which is represented by the well-known Traube-Herring curves; again, the height to which the vaso-motor centre drives the blood-pressure may be taken as representing the activity of the compression force.
When the compressing force rises above a certain limit the débâcle occurs—the vaso-motor centre retires from the fight, there is a rapid fall in blood-pressure, the medulla is emptied of blood, and both cardiac and respiratory centres share in the defeat (rapid pulse of poor volume and Cheyne-Stokes respiration).
These being the effects as exercised by compression on the bulbar centres, one must not omit to consider the results produced on the higher cortical centres. Anæmia is the feature and unconsciousness is the ultimate result, preceded by headache and drowsiness progressing on to stupor and coma. Intermediate between the stages of sleepiness and coma, one observes occasionally a stage of irritation—such as is pictured in many cases of typical middle meningeal hæmorrhage.
In fatal cases the respiratory centre gives out first, the heart often beating for some time after all attempts at respiration have ceased. In a case recently under my care, respiration ceased during the process of trephining. The patient was kept ‘alive’ for three hours by means of artificial respiration, and under such mechanical breathing the patient retained a good colour and the heart worked well. So soon, however, as efforts were relaxed, the pulse became weaker and weaker until further artificial respiration again restored the balance. This process was kept up till it was realized that the respiratory centre was ‘dead’.
From these facts, it may be assumed that the special symptoms of compression are dependent (a) on anæmia of the bulb—with corresponding cardiac, respiratory, and vaso-motor changes; and (b) on anæmia of the cortex—with unconsciousness.
Its symptomatology. According to Kocher, the following are the four stages of compression:—
1. The stage of compensation. A mild degree insufficient to seriously compromise the circulation. Cerebro-spinal fluid escapes into the spinal canal and some of the venous radicles are compressed. Some venous engorgement. Some headache, possibly some focal symptoms. Some mental dullness.
2. Stage of beginning compression. Beginning failure of the circulatory compensation. Headache pronounced, vertigo, restlessness, excitement or delirium. Objective symptoms of venous stasis—dilatation of the veins of the eye, both external and internal, œdema of the disk. Affection of the medullary centres, shown by a slowed pulse and a slight rise in temperature.