The stage of depression. The symptoms are evoked immediately on the receipt of the blow, the patient falling to the ground from lack of muscular control and loss of consciousness. The muscular system is completely relaxed, the limbs, when raised, falling helplessly to the ground. The face is deathly pale, the eyes usually open, fixed, and expressionless, the pupils equal, commonly dilated and responsive to light. The patient may be aroused by strong stimuli—pinching, shouting in the ear, pressure over the supra-orbital nerves, &c.
The pulse is small, slightly accelerated, and occasionally intermittent. The respiration is weak, shallow, and often irregular. The temperature is lowered, sometimes to such an extent that it cannot be registered on the thermometer. The surface of the body is cold and clammy, beads of sweat standing out on the brow. The deep reflexes are abolished. Some attempts may be made at swallowing when fluids are placed in the mouth.
Urine is often expelled at the time of the accident, and, more rarely, fæces may also be passed involuntarily.
The condition either gives place to that of reaction or the state of unconsciousness and collapse becomes more profound, in which case the prognosis is most unfavourable.
The stage of reaction. Weak, purposeless movements are observed and the patient may sigh heavily, mutter, or groan. This is followed by profuse vomiting, after which the temperature begins to rise, the body becomes warmer, and the patient recovers his senses either entirely or in part. The heart beats strongly, the pulse being full and slightly accelerated in rate. The carotid arteries are seen to pulsate forcibly, the face is flushed and moist. The patient is restless, and complains of severe headache, due in all probability to intradural hypertension. Under efficient treatment these symptoms of cerebral hyperæmia abate, the patient recovering quickly or slowly, according to the severity of the blow. Retrograde amnesia is often a conspicuous feature in the more severe cases, varying greatly in depth and character, seldom permanent.
In the more serious cases—those associated with severe cerebral injury—the pupils dilate fully and do not react to light. Corneal reflex is absent. The medullary centres gradually become exhausted, the pulse becoming smaller, increasing in rapidity, and finally unrecognizable. Respiration becomes weaker and often Cheyne-Stokes in character. Respiration ceases before the heart gives out.
Cerebral Irritation.
Its pathology. Sufficient evidence is supplied, both by clinical symptoms and by post-mortem examination, to show that brain irritation is dependent on definite brain lesions, these varying from ‘bruising’ to minor degrees of laceration. Bruising or contusion of the brain—evidenced by pia-arachnoid hæmorrhages and by cortical and subcortical hæmorrhages—is most prevalent in the frontal and temporo-sphenoidal regions. The same may be said with respect to laceration.
Its symptomatology. From the initial stage of concussion the patient passes into that of irritation, the reaction being of a rather violent type and accompanied by considerable rise of blood-pressure.
The patient lies curled up in bed, the lower extremities flexed at the hip and knee, the upper limbs bent across and partially covering the forwardly flexed head. He is exceedingly restless. Restraint is usually required. The eyes are tightly closed, and all attempts at pupillary examination are strenuously resisted. The patient groans, mutters, and uses language, perhaps suited to the occasion but not adaptable to polite society. Headache is severe, often referred to the frontal region. The skin is hot and dry—burning—the body temperature is raised whilst the pulse is accelerated and its tension increased. Both urine and fæces may be passed into the bed, not so much from loss of bladder and rectal control as from transitory moral perversion.