Traumatic Brain Injury

Rehabilitation for Everyday Adaptive Living, 2nd Edition

Jennie Ponsford, Sue Sloan, Pamela Snow

• Publisher: Psychology Press
• Year: 2012
• ISBN:
  9781136181382
• Edition: 1
• Topic: Psychologie
• Subtopic: Geschichte & Theorie in der Psychologie

Research into the rehabilitation of individuals following Traumatic Brain Injury (TBI) in the past 15 years has resulted in greater understanding of the condition. The second edition of this book provides an updated guide for health professionals working with individuals recovering from TBI.

Its uniquely clinical focus provides both comprehensive background information, and practical strategies for dealing with common problems with thinking, memory, communication, behaviour and emotional adjustment in both adults and children. The book addresses a wide range of challenges, from those which begin with impairment of consciousness, to those occurring for many years after injury, and presents strategies for maximising participation in all aspects of community life.

The book will be of use to practising clinicians, students in health disciplines relevant to neurorehabilitation, and also to the families of individuals with traumatic brain injury.

1 Mechanism, recovery and sequelae of traumatic brain injury

A foundation for the REAL approach

Jennie Ponsford

Introduction

Over the past three decades, there has been a significant growth of interest in the study of traumatic brain injury (TBI). The literature now abounds with studies of its epidemiology, pathophysiology, neuropsychology and outcome, and there have been numerous texts written on the subject. In spite of this, rehabilitation professionals remain uncertain in dealing with the challenging and complex problems presented by those who have sustained TBI, and most find it stressful. Moreover, outcome studies suggest that in spite of rehabilitative efforts, many people with severe TBI remain significantly handicapped, often causing great stress to their families. The reasons for this lie largely in the unique epidemiological, pathophysiological and neuropsychological characteristics of this population.

Before examining these characteristics more closely, it is important to be clear as to what is meant by the term “traumatic brain injury”. The Brain Injury Association of America describes a TBI as “an alteration in brain function, or other evidence of brain pathology, caused by an external force” (Brain Injury Association of America, 2011). Such an injury may result from a blow to the head from a relatively blunt object or from blunt impact of the head with a stationary object. TBIs may also result from penetration by a sharp instrument or a missile. These are termed open head injuries. However, penetrating injuries result in a somewhat different pattern of neurological deficit. The present text will deal with the consequences of TBI which have resulted from blunt impact, where the brain itself is not penetrated, otherwise known as closed head injuries. These represent approximately 70 per cent of all head injuries.

Epidemiology

Most studies suggest that the majority of moderate to severe TBIs result from motor vehicle accidents. Other causes include falls, bicycle accidents, assault, and sports injuries (Kraus and McArthur, 1999). In recent years the use of explosive devices in armed conflict has added a new mechanism of injury – blast injury, the effects of which are the focus of considerable current research interest, particularly in the USA (Tabar, Warden, and Hurley, 2006). It is difficult to obtain precise data regarding the incidence of TBI, due to variations in definition and methods of data collection. In the US, between 100 and 250 per 100,000 are admitted to hospital each year, and 20–30 per cent die (50 per cent in hospital and 50 per cent out of hospital). Other industrialised nations have similar rates (Bruns and Hauser, 2003). The Australian Institute of Health and Welfare has reported a rate of 107 TBIs per 100,000 population in Australia (Australian Institute of Health and Welfare, 2004; O’Rance and Fortune, 2007). Figures for China are relatively lower, at 56 per 100,000, and for South Africa and some European countries they are closer to 300 per 100,000 (Bruns and Hauser, 2003). Most studies suggest that approximately 20 per cent of TBI patients admitted to hospital have sustained moderate or severe head injuries (Bruns and Hauser, 2003), with the other 80 per cent representing mild injuries. Nevertheless, this represents a sizeable number. Moreover, a significant proportion (15–25 per cent) of those who sustain mild head injuries suffer ongoing cognitive difficulties (Carroll, Cassidy, Peloso et al., 2004b; Ponsford et al., 2000).

The highest overall incidence of TBI is in the age-group from 15 to 24 years, with other peaks in early childhood and in the elderly. In recent years there has been a rise in the proportion of those in older age groups sustaining TBI (O’Rance and Fortune, 2007). Most estimates indicate that between 1.5 and three males sustain TBI for every female, with the highest ratio evident in late adolescence/early adulthood, lower ratios in countries with less violence, and a more even ratio in the elderly (Bruns and Hauser, 2003). Studies focusing on other characteristics of the TBI population have suggested that a greater than average proportion have pre-existing maladaptive problems, such as psychopathology and substance abuse (Parry-Jones, Vaughan, and Cox, 2006; Rimel and Jane, 1984; Robinson and Jorge, 2002). TBI has also been shown to occur more commonly in the lower socio-economic classes, in people who are less educated and who are unemployed (Kraus and McArthur, 1999; Rimel and Jane, 1984).

Improvements in the acute management of TBI, particularly more rapid transfer to hospital and the use of measures to monitor and reduce intracranial pressure, have resulted in a reduction in mortality rates. The death rate from TBI in the US decreased from 25 per 100,000 to 19 per 100,000 between 1979 and 1992, although the death rate from firearm-related TBI has risen significantly in the USA (Bruns and Hauser, 2003). The declining death rate, together with the relative youth of those who sustain TBI, has led to a growth in the number of survivors of TBI in the community. They will be confronting their disabilities for decades in a society which still has a limited understanding of and facilities to cater for the needs of people with TBI.

Pathophysiology

Blunt trauma to the head associated with acceleration or deceleration forces results in a combination of translation and rotation, which may cause laceration of the scalp, skull fracture and/or shifting of the intracranial contents, with resultant focal and diffuse changes.

Skull fractures result from deformation of the skull at the time of impact. The majority of skull fractures are linear fractures, in which the area of impact is bent inwards and the surrounding skull is bent outwards. Fractures of the base of skull are common in the most severe head injuries. They carry a risk of intracranial infection via the sinuses or the middle ear and of cranial nerve injury. In a depressed skull fracture the bone has been pushed inwards beyond the level of the skull, and in a comminuted fracture the bone has broken into fragments. Both of these fractures may result in laceration of the cerebral cortex or haemorrhage and a possible focus for post-traumatic epilepsy and/or infection. They require surgery to lift and stabilise the bone segment (Roth and Farls, 2000). Fractures over the middle meningeal groove or the sagittal sinus may lead to the formation of an extradural haematoma.

The mechanisms whereby damage occurs within the brain tissue as a result of TBI are extremely complex, involving multiple, interactive pathological processes. These result in both focal changes, including contusion and haematoma formation, and diffuse changes, including diffuse axonal injury (DAI) and diffuse microvascular damage, as well as widespread neural excitation and metabolic changes (Povlishock and Katz, 2005). A distinction is drawn between primary and secondary brain injury resulting from blunt trauma, the former resulting directly from the trauma and the latter as a result of systemic complications, which are potentially treatable.

Primary brain injury mechanisms – Focal

Cerebral contusion

Contusions are haemorrhagic lesions resulting when acceleration/deceleration forces cause differential movements between the brain and the skull or at grey–white matter interfaces. They may occur at the site of impact, referred to as a “coup” injury, if local deformation has been sufficiently severe (Gaetz, 2004). Contre-coup contusions may be found on the opposite side to that of the impact, but are usually found on the crests of the gyri of the cerebral hemispheres, especially in those areas most likely to have contact with bony skull protuberances: the orbital plate of the frontal bone, the sphenoidal ridge, the petrous portion of the temporal bone and the sharp edges of the falces (Le and Gean, 2009). As a result, the basal and polar portions of the frontal and temporal lobes are most susceptible to contusions. However, contusions may also be found on the medial surfaces of the cerebral hemispheres and along the upper surface of the corpus callosum (Graham, 1999). They contribute to local neuronal destruction and ischaemia, or reduced blood supply, depriving neurons of oxygen and glucose.

Mechanisms of cell death occurring in contusional and pericontusional areas are termed necrosis and apoptosis. Necrosis occurs more quickly, as a result of membrane failure and ionic disruption, which degrade the neuronal cytoskeleton and cytoplasm and cause swelling and dilation of the mito-chondria. Apoptosis occurs slowly over a longer period, without disruption of the cell membrane. It may be caused by neural excitation, radical-mediated injury or a disruption of calcium homeostasis (Povlishock and Katz, 2005; Raghupathi, 2004).

Intracranial haematoma

Vascular injury may be seen as multiple tiny “petechial” haemorrhages throughout the cerebral hemispheres. Tearing of larger blood vessels at the time of impact results in bleeding inside the skull and the formation of a clot, which can eventually cause compression of the brain and ischaemia. This may lead to the development of coma after a delay or to a deterioration in conscious state, necessitating prompt surgical intervention to stop the bleeding and evacuate the haematoma. Intracranial haematomas are classified according to their anatomical location. An extradural haematoma results from bleeding between the skull and outer covering of the brain, known as the dura mater. This is most commonly a complication of a temporal skull fracture, where meningeal vessels have been torn. A subdural haematoma is a collection of blood between the dura mater and the arachnoid mater. The elderly are at increased risk of chronic subdural haematoma because of their increased risk of falls and the greater intracranial space caused by cerebral atrophy. A subdural hygroma is a collection of cerebrospinal fluid in the subdural space through a tear in the arachnoid mater. It develops days or weeks after injury, and may form after the evacuation of an acute subdural haematoma. A subarachnoid haemorrhage refers to bleeding between the arachnoid and pia mater. This may cause arterial spasm, leading to ischaemic brain damage. It can also lead to obstruction of the flow of cerebrospinal fluid, resulting in communicating high pressure hydrocephalus. An intracerebral haematoma is a haemorrhage within the brain caused by a deep contusion or tear in the blood vessels. As with other pathological consequences of TBI, intracerebral haematomata occur most commonly in the frontal and temporal lobes (Gennarelli and Graham, 2005; Le and Gean, 2009).

Primary brain injury: Diffuse neuronal change and axonal injury

The mechanical force of injury may cause more diffuse neuronal membrane disruption (Farkas, 2007). Some cells appear to be able to reorganise, restore their function and thereby survive this disruption, whereas others show persistent membrane dysfunction, with activation of cysteine proteases (calpain and caspase), causing rapid necrotic cell death.

Similarly, mechanical forces can result in scattered and multi-focal axonal change throughout the subcortical white matter, corpus callosum and brain stem, termed diffuse axonal injury (DAI). In the most severe injuries, axons may be torn and retract, expelling axoplasm and forming “retraction balls”. More commonly, mechanical strains cause focal alteration of the axolemma, or disruption of sodium channels, resulting in an influx of ions such as calcium, that disrupt the cytoskeleton. This results in progressive changes disrupting axonal transport and causing local swelling of the axon, followed by detachment from its downstream segment. Both myelinated and unmyelinated fibres appear to be vulnerable. These pro-cesses may take place over several hours or days after injury, creating a potential opportunity for intervention. Various therapies aimed at protecting the mitochondria, including the use of immunophilin ligands, cyclosporin A and FK 506 and hypothermia, are under investigation (Povlishock and Katz, 2005).

Shearing strains are thought to decrease in magnitude from the cortical surface to the centre of the brain (Ommaya and Gennarelli, 1974). They are enhanced along interfaces between substances of different densities and therefore DAI occurs most commonly in the grey–white matter junctions around the basal ganglia, the periventricular zone of the hypothalamus, the superior cerebellar peduncles, the fornices, fibre tracts of the corpus callosum, and in the frontal and temporal poles (Gaetz, 2004).

A consequence of DAI is that of downstream deafferentation or denervation. The downstream axon, disconnected from its sustaining cell body, undergoes wallerian degeneration which may take place over several months after injury. Downstream nerve terminals undergo neurodegenerative change.

Although neoplastic responses are not well understood, there is some evidence to suggest that, in the case of mild–moderate injury, diffuse deafferentation may result in sprouting of adjacent intact nerve fibres, leading to some recovery of synaptic input to the deafferented areas. However, in the case of severe injury, there appear to be maladaptive changes, with fibre ingrowth and changes in cytoarchitecture (Povlishock and Katz, 2005). These processes, and potential means of influencing them, are the focus of continuing experimentation.

Widespread metabolic changes also occur following TBI. Across the spectrum of injury severity, TBI is followed by a short-lived increase in glucose metabolism (a sign of metabolic stress), followed by a decreased rate of glucose metabolism which may last for days or weeks and shows some correspondence with the period of recovery and with outcome. Elevated lactate and glutamate are also evident and higher levels are associated with poorer outcome (Bergsneider, Hovda, and McArthur, 2001).

Petechial white matter haemorrhage

DAI is most commonly associated with injuries involving acceleration– deceleration, such as motor vehicle accidents. Findings on computed tomography or magnetic resonance imaging may include the presence of petechial white matter haemorrhage as well as non-haemorrhagic white matter lesions, diffuse oedema, and small subarachnoid and intraventricular haemorrhages (Povlishock and Katz, 2005). Deeper lesions are indicative of more severe injury (Blackman, Rice, and Matsumoto, 2003; Grados et al., 2001). Adams et al. (1989) refer to three grades of DAI: Grade 1 where focal haemorrhagic lesions are confined to the white matter of the cerebral hemispheres; Grade 2 where there is involvement of the corpus callosum; and Grade 3 where the dorsolateral upper brain stem is involved. However, lesser degrees of DAI may also be seen in some cases of mild head injuries (Bigler, 2008). Over time there is increasing atrophy, the extent of which is correlated with injury severity and outcome (Bigler, 2001a).

Secondary brain injury mechanisms

Both intracranial and extracranial complications may result in secondary brain injury, either as a consequence of cerebral ischaemia or distortion and/or compression of the brain/mass effect. Cerebral ischaemia, as a result of inadequate blood flow and consequent tissue hypoxia, is usually the ultimate cause of secondary brain damage associated with TBI. Hypoxic damage is frequently found in the border zones of areas supplied by the major cerebral arteries, particularly in the parasagittal cortex, the hippocampus, the thalamus and basal ganglia (Gennarelli and Graham, 2005). Intracranial complications may include the following:

Brain swelling

There are two mechanisms which lead to an increase in the volume of the brain following TBI. The first is an increase in the cerebral blood volume, termed hyperaemia, caused by hypoxia, hypercapnia, or obstruction of major cerebral veins as a result of cerebral oedema. The second is cerebral oedema, resulting from an increased volume of intra- or extracellular fluid in the brain tissue. Cerebral oedema may be caused by damage to the walls of cerebral blood vessels, accumulation of fluid within the cell as a result of ischaemia, increased intravascular pressure, or an obstruction to the flow of cerebrospinal fluid. These mechanisms may result in brain swelling of either a localised or a diffuse nature. Damage to the brain tends to be caused by a mass effect, with brain shift and/or raised intracranial pressure, leading to hypoxia/ischaemia.

Infection

Infection, which may develop in the subacute phase after TBI, is a com-plication associated with skull fracture. It can manifest itself in two forms: meningitis and cerebral abscess, causing raised intracranial pressure and/or brain shift.

Raised intracranial pressure

Increases in intracranial pressure (ICP) are a common consequence of the abovementioned intracranial complications, causing impairment of brain function due to reduction in cerebral perfusion pressure and consequently in cerebral blood flow, resulting in ischaemia, and brain shift. Uncontrolled intracranial pressure frequently causes diffuse ischaemic brain damage (Gennarelli and Graham, 2005). Cerebral autoregulation, or the ability of the brain to maintain a constant blood flow to the brain, may be impaired or lost under conditions such as increased intracranial pressure, ischaemia, inflammation or low or high mean arterial pressure, rendering the brain more vulnerable to ischaemia. Reductions in blood flow result in metabolic changes, which ultimately result in neuronal disintegration. Intracranial pressure and associated cerebral perfusion pressure are therefore routinely monitored in severe TBI cases.

Another potential consequence of raised intracranial pressure, haematoma and/or brain swelling is herniation. Subfalcine herniation occurs when one cingulate gyrus herniates across the midline. A more serious type is transtentorial herniation, where there is downward displacement of the parahippocampal gyrus and u...