Statements have recently been brought forward to the effect that concussion is in reality a mild type of compression. This view received at first sight some confirmation from the experiments of Koch and Filehne, who, from the application of consecutive slight blows to the heads of dogs, showed that each blow resulted in bulbar stimulation followed by bulbar depression. The blows being continued, the degree of stimulation decreased and that of depression increased until exhaustion and death resulted. During the periods of stimulation the pulse-rate slowed, during those of depression it increased.
It should be noted, however, that concussion, as observed in the human being, results from one sudden and violent blow. It may, I think, safely be assumed that, in such cases, the stimulating effect of the blow is entirely abolished in favour of an acute depression. And, as Archibald[35] says, ‘their records of respiration, pulse, and blood-pressure resemble far more closely the course of an increasing compression, with its gradual slowing of pulse and respiration and steady rise of blood-pressure, than that of concussion with its sudden standstill of pulse and respiration and fall of blood-pressure.’
In favourable cases the injury being of a comparatively mild nature, the vaso-motor centre soon recovers tone, and, as the result of previous depression, the vascular conditions are now reversed—the stage of depression giving place to the stage of reaction. The blood-pressure rises, the carotids pulsate forcibly, the face is turgid and flushed, the skin hot and moist, whilst the temperature rises, and the general cerebral hyperæmia is evidenced by headache, restlessness, and perhaps by delirium.
In the more severe cases the vaso-motor depression is unduly prolonged, or persists till death, the patient remaining concussed for a considerable period of time, or dying in that condition. In these fatal cases the post-mortem examination usually reveals brain laceration, but always evidences considerable engorgement of superficial cerebral veins, increase of cerebro-spinal fluid and œdema, both of the pia-arachnoid region and of the brain substance itself. These latter phenomena are accounted for by the fact that, insomuch as the venous pressure and cerebro-spinal tension are equal, the greater the engorgement of the cerebral veins the more extensive is the transudation of fluid into the pia-arachnoid and cerebral systems. In a fatal case of concussion—recently under my care—the surface of the cortex, when exposed by operation, was obscured by a layer of œdematous pia-arachnoid 1⁄4 inch in depth.
Arguing from the presence of the very definite pathological changes observed in all fatal cases—contusions, lacerations, hæmorrhages, and œdema—one may arrive at the conclusions (1) that lesions of a similar but less serious nature are existent in the serious but non-fatal cases, and (2) that the prolongation of the stage of depression is directly dependent on the presence of such lesions.
On investigating the numerous cases that come under the care of the surgeon, certain features present themselves which are not always readily explained on the definition of concussion as given above. Thus, the variability of the symptoms evinced in cases of concussion admitted into hospital are well exemplified by the following table, compiled from a consecutive series of 50 cases admitted into St. Bartholomew’s, diagnosed and treated as concussion:—
| 12 cases in the hospital for 7 days or less (cerebral shock only). | |||||
| Temperature on admission: | 8 | subnormal. | |||
| 2 | normal. | ||||
| 2 | slightly raised. | ||||
| Pulse on admission: | 3 | subnormal. | |||
| 3 | normal. | ||||
| 6 | accelerated. | ||||
| 26 cases detained for 7 to 10 days (probably cerebral shock only). | |||||
| Temperature on admission: | 6 | subnormal. | |||
| 9 | normal. | ||||
| 11 | slightly raised. | ||||
| Pulse on admission: | 4 | subnormal. | |||
| 12 | normal. | ||||
| 10 | accelerated. | ||||
| 9 cases detained for 14 to 21 days (probably cerebral contusion). | |||||
| Temperature on admission: | 2 | subnormal. | |||
| 3 | normal. | ||||
| 4 | slightly raised. | ||||
| Pulse on admission: | 6 | subnormal. | |||
| 1 | normal. | ||||
| 2 | accelerated. | ||||
| 3 cases detained for 21 to 30 days (certainly cerebral contusion). | |||||
| Temperature on admission: | 1 | normal. | |||
| 2 | slightly raised. | ||||
| Pulse on admission: | 1 | subnormal. | |||
| 1 | normal. | ||||
| 1 | accelerated. | ||||
Still, when all is considered, concussion and compression are but ill-defined from one another, both in their clinical and pathological aspects. The more indefinite cases of concussion are probably such as border on compression, the increasing œdema gradually carrying the patient across the border line between the two conditions.
In the present state of our knowledge respecting concussion or cerebral shock it may, I think, be accepted (1) that concussion is dependent on an acute inhibition or paralysis of the vaso-motor centre; (2) that the milder cases are unassociated with any pathological visible changes; (3) that the prolongation and severity of the depression stage are directly proportionate to the extent of the brain lesion, such lesions varying from œdema and contusion to extensive hæmorrhages and lacerations.