FREE CHAPTER from ‘A Practical Guide to Catastrophic Brain Injury Claims’ by Pankaj Madan


Let us get one thing clear first of all. “Head injury” does not mean “brain injury”. Head injury can mean injuries not to the brain but injuries to the scalp, skull, face and jaw.

Head injury is therefore an all-encompassing term of which brain injury is a sub-set. Brain injury from trauma is normally what personal Injury lawyers are dealing with and the preferred term is “traumatic brain injury”. Where we are dealing with traumatic brain injury which is not at first sight obvious or apparent then the term “STBI” or subtle traumatic brain injury can be used. It does not imply however that the brain injury is necessarily minor or is not having substantial and very serious effects upon the functioning of the individual.

Injury to the brain can however occur as a result of a number of conditions including:

  • Trauma
  • Cerebrovascular events
  • Degenerative disorders
  • Hydrocephalus
  • Toxicity
  • Infection
  • Tumours
  • Oxygen deprivation
  • Metabolic and endocrine dysfunction
  • Nutritional deficiencies

What is a traumatic brain injury?

The first problem is that a head injury and a brain injury are often confused. One can of course sustain an injury to the “head” without sustaining injury to the brain. There may conversely be no visible injury to the “head” yet the brain itself may have sustained an injury.

Traumatic brain injury means trauma to the brain as a result of some external force to the brain usually with some diminished or altered state of consciousness. This does not mean that somebody has to be unconscious in order to have demonstrated or suffered a brain injury.

The ICD11, one of the international diagnostic manuals used by doctors, recognises that head injury can be anything from a superficial injury to the head through to an intra-cranial injury. Intra-cranial injury can range from concussion to traumatic amputation of the head.

Traumatic Brain injury (“TBI”) is global world health problem and is a major cause of disability. According to the World Health Organisation, traumatic brain injury will soon exceed many diseases as the cause of major disability and death.

In the UK there are roughly 400 incidents of traumatic head injury per 100,000 of population in any one year and around 240 per 100,000 in the EU as a whole. Overall, males are twice as likely than females to experience a TBI and the risk of traumatic brain injury is particularly high in relation to children. The mortality rate is between 5 and 10 per 100,000 in the UK.

The leading cause of traumatic brain injury is consistently reported as being road traffic accidents, around 21% in the UK and 25% in the USA.

There is some evidence that genetic factors may pre-dispose some people to a poorer outcome following such injury. Some research has shown that the apolipoprotein E has an effect on the deposit of amyloid beta-protein in the cerebral cortex and this is involved in neuro-degeneration. Some people more prone to produce this lipo-protein have been associated with a doubling of likelihood of a poorer outcome at 6 months following a traumatic brain injury.

Types of traumatic brain injury

These may be closed or blunt where the dura mater and brain are not penetrated.

Or open or penetrating where the dura and brain are penetrated.

Skull fractures or their absence are not always of significance. They do indicate that a substantial amount of force hit the head but of course the area over which the force is distributed may mean that the skull in fact fractures.

Skull fractures may result in CSF leakage however and are an important source of infection and air bubbles. The orbital roof is commonly fractured when for example a person falls backwards hitting the occiput on a hard surface with the shock wave passing through the skull and fracturing the orbital roof which is pretty thin.


Coup and contrecoup

Coup is the expected movement of the brain when for example it decelerates. The rebound movement of the brain, for example rearwards again is the contrecoup.

Haemorrhage which is intra-cranial, inside the skull can be outside the dura or inside the dura. If it is outside or above the dura (see Chapter 1) it is known as an extradural haemorrhage. This is as a result of a direct impact to the skull.

If it is beneath the dura it is known as a sub-dural haemorrhage.

It is important of course to remember that the force does not have to be applied to the skull in order for a brain injury to occur. The brain is of course for example in a motor vehicle usually moving. When it decelerates suddenly the brain continues to try and move and strikes the inside of the hard skull, the calvarium. Contusions consist of haemorrhage and can carry on bleeding for hours causing a raised intra-cranial pressure. It is a particular problem the older the person gets as the brain atrophies with age and allows for even greater movement within the skull.

Sub-dural haemorrhage which is present soon after the injury is known as “acute”. If it is only present 1-2 weeks later it is called “sub-acute” and if it is present more than 2 weeks later it is called “chronic sub-dural haemorrhage”.

Sub-arachnoid haemorrhage is particularly serious. This often results from an impact to the head and with contusions and lacerations. A laceration around one of the arteries feeding the brain stem often results in immediate collapse and is often fatal. It is a marker for catastrophic brain injury and consequent epilepsy.


Diffuse Injury

Diffuse Axonal Injury is altogether very different and it is very important in terms of brain injury. Diffuse axonal injury can be very serious, even fatal of course and does not necessarily equate with a subtle traumatic brain injury although is often referred to in that context.

Diffuse Axonal Injury (“DAI”) is widespread damage to the axons within the brain. Trauma is an accepted cause of DAI as is hypoxia (lack of oxygen to the brain) and hypoglycaemia (lack of nutrition to the cells). DAI caused by trauma is different however, and it can be caused by rapid acceleration or deceleration of the head particularly where there is a rotational movement of the head.

Traumatic axonal Injury can cause very severe brain injury resulting in death. In these cases it causes immediate unconsciousness and can result even in persistent vegetative states (PVS). In these severe cases there will be damage to the small blood vessels resulting in spots of blood being present on the MRI scans. These are called “Petechiae” or “petechial haemorrhages”.

Damage to the axons results in swollen, torn and damaged fibres in the white matter of the brain. Over time, damaged axons may die and there may be shrinkage of the white matter. Ironically therefore, the effects in more minor cases of DAI may take some time to become immediately apparent. Damage to these long fibres can also cause an influx of enzymes and damage to proteins disrupting axonal transport mechanisms and resulting in accumulation of proteins.

The relationship between white matter damage and the effect upon higher executive functions is proving to be very complex to medical science.

Research by Kinnuen, Greenwood and Powell et al. reported in the medical Journal, “Brain” (Brain 2011:134; 449-463) suggests that although chronic and widespread abnormalities of white matter are identifiable following traumatic brain injury, the impact of these changes on cognitive function is likely to depend on the precise damage to key pathways that link nodes in the brain network supporting high level cognitive functions.

The frontal lobe at the point where it rests on the cribriform plate (to the rear of the nasal bones) is particularly vulnerable to axonal injury from contrecoup forces following a whiplash type injury mechanism. This is the area which controls executive function and personality. The olfactory bulb, which is responsible for sense of smell surrounds it.

The Corpus Callosum

This is the largest single bundle of axons crossing over from the left to the right side of the brain and linking the two. The structure of the brain makes it prone to injury during certain types of impact, particularly rotational.

The falx is a stiff cartilage-like structure running down the fissure dividing the left and right hemispheres of the brain. At the centre of the brain is small vault-like structure known as the “central sulcus”. The large bundle of axons, the corpus callosum cross over from the left to the right side of the brain deep inside the brain.

Comprehensive studies have been performed by David Camarillo and his team on American football players to measure the forces which are transmitted as a result of impacts and in particular head rotation. [1]

They used a mouthguard fitted with sensors to detect how the head actually moved when struck. This allowed them to study live subjects who commonly suffered concussion as a result of impact, namely American Football Players.

A player struck to the lower left side of the mask suffered a whiplash type effect. First the head went to the left and then whipped violently to the right.

Computer simulations measured the stretch on the known properties of the brain tissue.

Contrary to the expectation of surface related coup-contrecoup injuries the key thing to notice from the study is that the falx appeared to rapidly transmit the highest forces down the fissure into the central sulcus where the single largest axon bundle was. This is the corpus callosum. This caused a dissociation between the right and left side of the brain and symptoms of traumatic brain injury.

Diffuse Vascular Injury

In very severe cases of acceleration/deceleration of the brain there can be widespread petechial haemorrhaging. These injuries are generally fatal.

Persistent vegetative and minimally conscious states

These are the most severe forms of brain injury short of death. PVS and MCS are not the same.

A vegetative state (VS) will have the following characteristics:-

  • Sleep/wake cycles with spontaneous eye opening;
  • Preserved brain-stem function so that circulation and respiration are spontaneously maintained;
  • No awareness of the environment or of themselves;
  • Absence of response to sensory stimulus;
  • Absence of language comprehension or meaningful expression.

If the condition lasts longer than 8 weeks it is then a persistent vegetative state (“PVS”). This does not necessarily mean that it is not reversible however.

However, once 6 months has passed then it is usually classed as permanent albeit there remains a possibility though not a probability of improvement.

A minimally conscious state differs from a vegetative State (VS) because:

  • There is limited but defined awareness of the environment
  • There is a sub-category of MCS minus patients and MCS plus patients
    • MCS minus show non-reflexive movements sometimes when stimulated;
    • MCS plus show more complex behaviours, following commands for example despite profound cognitive impairment.

Improvement from PVS and MCS

Age is an important factor. In relation to PVS- Patients over 40 years of age show worse improvement than those under 40 years of age. At one year according to a meta-study:-

  • 33% had died
  • 15% remained in a PVS
  • 28% were severely disabled
  • 17 % were moderately disabled
  • 7% had made a good recovery.

Patients with a MCS show much more variable levels of recovery but almost all of them continue to need life-long care.

Hidden Consciousness (CMD)

The latest research from Columbia University, New York, considers that around 15% of “coma” patients may have Cognitive Motor Dissociation (CMD) but are not actually in a coma. These are patients who are processing at least some of what is happening around them but cannot physically respond. CMD is a break between understanding and responding. The diagnosis requires advanced equipment and training. The team have found however that simpler equipment can also diagnose the condition, structural MRI to look or brain lesions combined with functional EEG (Electro-encephalogram). Using both they were able to identify two patterns of brain lesions only seen in CMD patients. The lesion patterns were not surprisingly in areas of the brain important for motor output but comprehension and arousal centres of the brain were intact. CMD patients have a higher chance of recovery but there is a risk that failure to identify CMD patients could mean that life-sustaining therapies are withdrawn prematurely. The drug Amantadine has been shown to help recovery in patients in a vegetative or minimally conscious state and the next steps are trial this in patients with CMD to see if it aids recovery there too.



In summary:-

Primary brain injury is usually caused by either a direct blow to the head or more usually in our experience of acceleration/deceleration forces on the brain leading to:-

  • Contusional injury (bruising of the brain)
  • Coup (at the site of the impact)
  • Contre-coup (at the opposing side of the impact)
  • Diffuse axonal injury (DAI) which is the shearing or stretching of axons or fibres connecting neurones or nerve cells together
  • Sometimes but not always haematoma or loss of blood.

After primary injury, secondary injury can occur especially in more severe head injury, as a result of oedema (swelling due to fluid), hypoxia (lack of oxygen to the nerve cells) and infection.

  • PVS and MCS are the most severe forms of brain injury and generally outcomes are very poor with lifelong support needed albeit with substantially reduced life-expectancy.
  • There is a concern about hidden consciousness called CMD. Up to 15% of “coma” cases may be a case of hidden consciousness with an inability to communicate but processing is still occurring.


[1] See “Why helmets don’t prevent concussion and what might”. TED Talk 29th September 2016.