Minor head injuries - a major problem
By Dr Jon Simcock
Head injuries are familiar to everyone, commonly resulting from body contact sports such as rugby and boxing, from accidental falls and from motor vehicle/bike accidents. While these are usually “mild” on a neurosurgical scale of severity, the effects on the person and family can be devastating.
The brain injury we are considering is due to movement of the brain within the skull by either of two mechanisms. Firstly, if the head is hit by a blunt object ( e.g. another person’s knee in rugby or the opponent’s fist in boxing), the skull suddenly accelerates and the inertia of the brain within the skull results in tearing of the nerve fibres in the brain region which is relatively fixed in relation to the skull (the upper brainstem) when the cerebral hemispheres move within the skull. Secondly, in a fall, when the moving head hits the ground (suddenly decelerating), the brain continues to move inside the skull with similar stretching/tearing (shearing) of the nerve fibres of the upper brainstem. In addition, there may be direct brain injury under the point of impact of the blow, or opposite to the point of impact (often the front of the temporal lobes and/or the undersurface of the frontal lobes).
The shearing injury to the upper brainstem is the cause of the immediate loss of consciousness in knocks to the head – there is no delay, not even a few seconds. While loss of consciousness is a usual feature of concussion, significant brain injury can be caused without it, when the symptoms are disorientation, confusion and impairment of memory.
Neurosurgeons grade the severity of a closed head injury by the Glasgow Coma Scale (GCS). This is an assessment based on three clinical observations - eye opening (1-4 points), best verbal response (1-5 points) and motor response (1-6 points), shown in the accompanying table. The categories of severity are Mild 13-15, Moderate 8-12, Severe 3-7. The time after the injury of this assessment is clearly important – most people (not neurosurgeons) would regard a person with a GCS of 13, three or four hours after an accident, as having had a severe head injury. This emphasizes that severity scales should be used only in the context for which they were designed.
GLASGOW COMA SCALE
To voice 3
To pain 2
Obeys commands 6
Localizes pain 5
Total 3 - 15
Another measure of the severity of the injury is the duration of the loss of consciousness assessed by an eyewitness – the time from the impact to when the person opens their eyes, gazes at objects and talks. From the patient’s point of view, consciousness returns with the restoration of memory. The patient may walk and talk for quite a time before memory returns, so that observed loss of consciousness lasting 10 seconds can be followed by a period of 15 minutes of amnesia, so that the patient considers he has been unconscious for 15 minutes. This time to recovery of continuous memory is another indication of the severity of the brain injury. Retrograde amnesia is the loss of memory of events occurring before the injury. For example, in a motor vehicle accident, the few seconds before the impact may not be remembered and the next memory may be of being put into the ambulance 30 minutes later, although the observed period of loss of consciousness was just a few seconds. This person was concussed and could then have post-concussion symptoms. Complete recovery could occur in anything from a week to several months. An MR scan would be expected to be normal.
While concussion is the most common and often the only result of a closed head injury, other types of injury may occur.
1. A mild head injury can trigger an attack of migraine – this is traumatic migraine and starts immediately after the blow to the head. For example, a rugby league player would develop tingling in the right hand after a stiff-arm tackle. The tingling numbness would then spread to the right side of the face and tongue over several minutes and he would then be unable to say what he wanted to. These symptoms would resolve in about 15 minutes and he would then have a throbbing headache with vomiting lasting three or four hours and would then be perfectly normal. He thought he was having minor strokes, but this was traumatic migraine. He made a confident diagnosis of the same disorder in his son 15 years later, who had similar episodes, again when playing rugby league. Traumatic migraine seems more common in children and adolescents, and is often misdiagnosed as concussion. It is not usually an indication for a stand-down period from playing sport and even repeated episodes do not result in persistent brain damage.
2. In the elderly, a minor head injury can cause a sub-dural haematoma (bleeding between the membranes covering the brain within the skull). This gives increasing headaches and fluctuating drowsiness over several days or weeks, when steady improvement is the usual pattern with uncomplicated concussion.
3. An injury such as falling backwards and hitting the back of the head on concrete can cause relatively minor concussion but the movement of the brain within the skull can shear off the delicate nerve fibres transmitting the sense of smell from the top of the nasal passages – this can result in the permanent loss of the sense of smell.
4. Closed head injuries can also damage the part of the inner ear concerned with balance, so that the patient has vertigo (a feeling of spinning) on moving his or her head. This can result in anxiety and secondary symptoms and needs to be differentiated from the feelings of muzziness or lightheadedness that can be a part of concussion.
Some patients continue to have a variety of symptoms after head injury – the post-concussion syndrome.
These symptoms include headache, poor concentration, slowness of thinking, blurred vision, dizziness, fatigue, sleepiness, insomnia, irritability and sensitivity to loud noises. Mostly, there is gradual improvement in all of these symptoms with full recovery. During the recovery period, short bursts of mental and physical activity are appropriate, interspersed with rest periods.
It will be noted that the post-concussion symptoms are similar to those of post traumatic stress disorder and both disorders can be concurrent. An example would be the innocent victim of a MVA having a closed head injury causing concussion, together with the stress and resentment of being hit by a drunken driver, being out of work and with consequent financial worries resulting in post-traumatic stress disorder. Post-traumatic migraine can add to the difficulties, delaying recovery.
Another consequence of a closed head injury with concussion can (rarely) be the second-impact syndrome.
If a person who has not recovered from concussion has a second head injury, then acute brain swelling can occur with disastrous consequences. Brain swelling is not a usual feature of concussion.
Repeated concussions can led to progressive dementia later in life – this is well recognized in professional boxers (the punch-drunk syndrome) occurring in about 20% of professional boxers. A similar disorder has been described with autopsy findings in four professional footballers in America’s National Football League (NFL). Autopsy findings showed characteristic microscopic changes in the brains, but with some similarities to the changes seen in Alzheimer’s disease. The NFL is conducting a study on the neurocognitive effects of concussion, investigating 120 players who retired between 1984 and 1996. This group will be compared with a group of men who played football in high school land college, or for less than one season in the NFL. There could be a problem establishing the number of concussions – one of the four footballers autopsied with marked brain abnormalities, had only one concussion recorded by the NFL but an independent interview had recorded that he “lost count after 15” concussions.
A recent study of amateur boxers in the USA showed surprising findings. 14 boxers had lumbar punctures one week after a fight and again three months later. The results were compared with 10 healthy males who had no head injury (controls). Several proteins in the cerebrospinal fluid obtained at lumbar puncture were measured. These proteins were derived from damage to axons (nerve fibres) in the brain. One week after boxing, the levels were four times higher in the boxers than the controls and in the boxers hit the most and hardest, the value was seven times higher. After three months without an intervening fight, the values for all the brain-derived proteins returned to normal. While one study of amateur boxers (who had not been knocked out) showed slower reaction times four days after their fights, another study showed that cognitive function two hours after a fight was no different from that before the fight.
The aim of boxing is to render the opponent unconscious by damaging the brain – the earlier in the bout, the better. A boxer’s skill is denoted not only by his win/loss/draw results but also by the number of knockouts and in which round. While only a few boxers suffer subarachnoid or subdural haemorhages as a result of the blows to the head, many suffer some head injury and a few develop progressive dementia. Because there is evidence of brain damage in amateur as well as professional boxers, it should be questioned whether it is appropriate for a government agency to provide funds for boxing and whether school principals should foster boxing in their schools.
Concussion and the post-concussional syndrome are frequent and important : late effects do not occur except when there are repeated concussions. This aspect of minor head injuries requires further research.
Dr Jon Simcock FRCP, FRCAP, is the Neurological Foundation’s Medical Adviser