Chapter 3 Acquired brain injury
trauma and pathology
Introduction
Discussion of physical management is confined to rehabilitation, recovery and adjustment. The management of ABI in the context of terminal illness is not addressed. Physiotherapists most commonly encounter individuals who have survived injuries at the more severe end of the spectrum: those who are admitted for extended periods of hospital care and those who continue to have significant impairments of motor performance following hospital discharge. However, the effects of brain injury extend far beyond overt physical disability (Table 3.1) and may impact on both family members and wider social networks. An adequate understanding of this extended effect is essential if physiotherapists are to work effectively with other health- and social-care professionals to assist a person’s re-establishment within the community.
Table 3.1 Definitions of traumatic brain injury
| Organization | Definition |
|---|---|
| Medical Disability Society, UK | Brain injury caused by trauma to the head (including the effects upon the brain of other possible complications of injury notably hypoxaemia and hypotension, and intracerebral haematoma) |
| National Head Injury Foundation, USA | Traumatic head injury is an insult to the brain, not of degenerative or congenital nature but caused by an external force, that may produce a diminished or altered state of consciousness, which results in impairment of cognitive abilities or physical functioning. It can also result in the disturbance of behaviour or emotional functioning. These impairments may be either temporary of permanent and cause partial or total functional disability or psychosocial maladjustment. |
Traumatic brain injury
Mechanisms of injury
The brain has most of its mass in two large cerebral hemispheres, above the narrower brainstem and spinal cord (Nolte, 2001a). The brain and spinal cord are suspended within three layers of membranes known as the meninges and are further protected by a layer of cerebrospinal fluid between the inner two layers, the arachnoid and pia mater. The outer layer, the dura mater, is the most substantial layer and provides most of the mechanical strength of the meninges (Nolte, 2001b). The dura mater is attached to the inner surface of the skull. During normal activities the brain is constrained to move with the head but as it is not directly anchored within the skull this does not apply during sudden, swift movements or high-energy impacts. The brain substance is composed of cells and axonal connections forming areas of different densities that move and respond to force in different ways. Thus, the brain is free to move independent of the skull and in the presence of high energy it does so in an irregular manner, causing stretching and shearing of brain tissue. Further damage is inflicted on the soft brain structure as it moves across the irregularities on the internal surface of the skull (Jennet & Teasdale, 1981).
Types of injury and associated damage
Primary damage
External forces are expressed via three main mechanisms of primary brain injury:
Closed injuries can result in local impact, polar impact, shearing, laceration, axonal or blood vessel damage. Local impact damage occurs immediately below the site of impact and can affect the scalp and meninges, as well as the brain substance in different measure, depending on the velocity of the impact and the flexibility of the skull. The brain may collide with the skull at the opposite pole to the site of primary impact and oscillate between the two, producing additional shearing damage. Where shearing forces affect the long axonal tracts, such as in hyperextension or rotational injuries, axons may be stretched or severed within their myelin sheaths (Adams et al., 1977). This is known as diffuse axonal injury (DAI). When DAI is widespread it is associated with severe injury but has also been shown to occur in mild injuries (Povlishock et al., 1983; Yokota et al., 1991).
Lacerations most commonly occur adjacent to the internal areas of the skull that are irregular, producing damage to the frontal and temporal lobes of the brain (Currie, 1993). Perfusions studies in mild injuries have identified frequent frontal, temporal and midbrain lesions (Abdel-Dayem et al., 1998; Abu-Judeh et al., 1999). Hyperextension injuries can cause damage to the carotid or vertebral arteries interrupting blood flow as a result of dissection or occlusion (Auer et al., 1994; Sprogoe-Jakobsen & Falk, 1990). Cerebral vessels can also be torn or ruptured and result in a local collection of blood. When this occurs in the immediate aftermath of an injury it is known as an acute haematoma. A slower accumulation of blood, known as a chronic haematoma, is most frequently found in the very young or in older adults.
Secondary damage
Secondary damage may be aggravated by infection or complications associated with systemic dysfunction, which may result from the effects of the brain injury or be caused by coexisting injuries. Around 40% of severely injured patients will have other significant injuries (Gentleman et al., 1986).
Epidemiology of traumatic brain injury
Studies reporting the incidence of TBI in Western countries produce a range of values of around 200–300 new cases presenting for medical evaluation per 100 000 population each year; for example, in the USA (Sorenson et al., 1991), the UK (Jennett & MacMillan, 1981; Tennant, 2005) and Australia (Hillier et al., 1997). The peak risk of injury is between the ages of 16 and 25, declining until late middle age before beginning to rise again around age 65 (Sorenson et al., 1991). Males are almost three times more likely to be injured and to have more severe injuries, resulting in an injured survivor ratio of around 2:1 male to female (Kraus et al., 1996). In 1998 the number of people living in the UK with significant disability after TBI was estimated to be between 50 000 and 75 000 (Centre for Health Service Studies, 1998). The figure given by the Department of Health in 2005 for those living with long-term effects of TBI in England was significantly higher at 420 000 (Department of Health, 2005).
Risk factors and preventive measures
Sporting accidents and falls are the primary causal factors for those under 20 years, with transport accidents accounting for less than 15% of injuries in one study focusing on an adolescent sample (Body et al., 1996). In adult populations transport accidents are commonly responsible for around 50–60% of injuries, with falls and assaults being the other major causal factors. In older adults there is a very high level of falls and a more even level of occurrence across genders (Miller et al., 1990).
Injury prevention can be considered on three levels (Kraus et al., 1996):
Positive effects have been reported for motorcyclists wearing helmets (Gabella et al., 1995; Kraus et al., 1994) and following the introduction of compulsory bicycle helmets in the USA (Thompson et al., 1989) and Australia (McDermott, 1995). Increasing awareness of the potential for enduring problems following minor brain injury and the cumulative effects of repeated minor trauma has led to the development of guidelines for the management of concussion injuries in sport (Fick, 1995; Leblanc, 1995; Leclerc et al., 2009; McCrory et al., 2005). However, there remains a great deal to do in terms of educating health-care providers, and youth and sports organizations to ensure that guidelines are followed and the correct advice given (Genuardi & King, 1995).
The Pashby Sports Safety Concussion website (Leclerc et al., 2009) gives definitions, explanations and advice, so that the effects of concussion can be recognized by those involved in sport at any level and to encourage return to participation to be appropriately paced. There is also now an internatioanlly agreed method of post concussion evaluation, the Sport Concussion Assessment Tool or SCAT (McCrory et al., 2005).
In terms of individual risk factors, substance misuse and, particularly, exposure to alcohol are widely recognized as prominent contributory factors in accidental (Jennett, 1996) and violent injury (Drubach et al., 1993). However, although there is some evidence that withdrawal from chronic alcohol use may exacerbate toxic cell damage following trauma, the net effects of the presence of alcohol at the time of injury at an individual level have not yet been defined (Kelly, 1995). There is emerging counter-intuitive evidence of no specific negative impact of alcohol on cognitive performance (Lange et al., 2008) or functional status (Vickery et al., 2008). There is some evidence of a relationship between previous alcohol abuse or dependency and disorders of mood and emotional disturbance following TBI (Jorge et al., 2005) and that having a first injury associated with drinking alcohol is predictive of recurrent TBI (Winqvist et al., 2008).
Measures and diagnoses of severity
Coma
Coma is defined as ‘not obeying commands, not uttering words and not opening eyes’ (Teasdale & Jennett, 1974). The Glasgow Coma Scale (GCS; Teasdale & Jennett, 1974, 1976) is the most widely used measure of depth and duration of coma. The GCS has three subscales, giving a summated score of 3–15:
Although a general impression of a person’s conscious level can be gleaned from a summated score, retaining the scores at subscale level gives a more accurate clinical picture. For example, knowledge of the lowest motor response rating and the pattern of improvement over time can provide physiotherapists with a valuable insight into the initial severity of damage to brain tissue associated with physical performance. Regarding summated GCS scores the convention is to categorize injuries into mild, moderate or severe (Table 3.2) using the lowest score in the first 24 hours.
Table 3.2 Traumatic brain injury severity: lowest summated Glasgow Coma Score in the first 24 hours post injury
| Grade | Summated GCS Score |
|---|---|
| Mild | 13–15 |
| Moderate | 9–12 |
| Severe | 3–8 |
GCS, Glasgow Coma Scale.
After Bond, 1986
Duration of coma is also used as an indicator of severity, where coma is generally numerically defined as a GCS score of 8 or less (Bond, 1990). This convention introduces a further grading of very severe (Table 3.3), reflecting the increasing knowledge that may be gained from longitudinal review.
Table 3.3 Traumatic brain injury severity: duration of coma
| Grade | Duration of coma (GCS ≤ 8) |
|---|---|
| Mild | < 15 minutes |
| Moderate | > 15 minutes, < 6 hours |
| Severe | > 6 hours, < 48 hours |
| Very severe | > 48 hours |
GCS, Glasgow Coma Scale.
After Bond, 1986
Postcoma states (vegetative and minimally conscious states) are discussed below (see ‘Loss of consciousness’).
Posttraumatic amnesia
The definition and assessment of PTA remain controversial. The original concept was developed by Russell and taken to be the period from injury until the return of day-to-day memory on a continuous basis (Russell, 1932). Most analyses now identify disturbances in three domains: orientation, memory and behaviour. For example, ‘the patient is confused, amnesic for ongoing events and likely to evidence behavioural disturbance’ (Levin et al., 1979, p. 675). However, Russell’s categorization of levels of severity is still used today (Table 3.4).
Table 3.4 Traumatic brain injury severity: duration of posttraumatic amnesia
| Grade | PTA |
|---|---|
| Mild | < 1 hour |
| Moderate | > 1 hour, < 24 hours |
| Severe | > 1 day, < 7 days |
| Very severe | > 7 days |
PTA, posttraumatic amnesia.
From Russell W.R., Cerebral Involvement in Head Injury: a study based on the examination of two hundred cases (1932), published by Oxford University Press. Reprinted with permission.
Tate and colleagues (Tate et al., 2000) discussed the relative merits of currently available scales for prospective assessment of duration of PTA, addressing issues of orientation and memory, and highlighting in particular the difficulties in assessing the memory component. Andriessan and colleagues suggest that the memory component is best assessed by a memory test that incorporates the free recall of words after a long delay (Andriessen et al., 2009). Retrospective assessment of PTA duration has been shown to be as reliable as prospective assessment in a severe population (McMillan et al., 1996), although Gronwall and Wrightson (1980) found that one-quarter of mildly injured patients changed their estimation at a second interview after 3 months.
Service provision
Improvements in surgical techniques and medical management, particularly since the 1970s, have resulted in substantially improved survival rates, and there is clarity and consensus on many medical management issues. Precise guidelines for the early management of those who sustain a TBI are now available, for example, the Scottish national clinical guideline (Scottish Intercollegiate Guideline Network, 2009) and the English National Institute for Health and Clinical Excellence (NICE) guideline (National Institute for Health and Clinical Excellence, 2007). However, services beyond the acute phase have been very slow to develop in the UK (see Campbell, 2000a, 2000f, for discussion) and while there are areas of good practice, there has been a growing recognition of the geographical inequalities and overall inadequacies of current provision (House of Commons, 2001) and some policy action to standardize and improve service delivery (Department of Health, 2005).
Worldwide, a number of models of service provision have been proposed, based on clinical experience and available evidence (Burke, 1987; Eames & Wood 1989; McMillan & Greenwood 1993; Oddy et al., 1989). Across these proposals there are a number of recurring themes, including the need for: organizational integration; interdisciplinary team work; professionals with advanced knowledge and skills; and a systematic programme of service evaluation and innovative research (Campbell, 2000f). Furthermore, there is acknowledgement of the need for multiple service components across health and social care, including options for supported living, and for services to be flexible in response, so that individuals may access them at a time of need and on more than one occasion, if appropriate (Department of Health, 2005).
Principles of acute management of traumatic brain injury
During the initial evaluation, movement of the cervical spine is minimized until any fractures have been excluded. Where appropriate, prophylactic antibiotic therapy is commenced immediately (Bullock & Teasdale, 1990a, 1990b). Except for the management of immediate seizures, the routine early use of anticonvulsant therapy is not now recommended (Hernandez & Naritoku, 1997).
Patients who exhibit breathing difficulties are assisted by intubation and ventilation (Bullock & Teasdale, 1990a). In addition, elective ventilation is often the treatment of choice in the presence of facial, chest or abdominal injuries, and for those with a summated GCS score of less than 9. Ventilation is usually achieved via endotracheal tube and tracheostomy is only performed where facial or spinal fractures determine this course of action or in the few cases when respiratory support is required over a more extended period. Even when ventilation is not indicated, oxygen therapy is recommended to help meet the injured brain’s increased energy requirements (Frost, 1985).
Those with significant injuries are at risk of breakdown of the normal process of cerebral autoregulation that ensures blood flow to the brain is consistently maintained, independent of the normal fluctuations in systemic blood pressure (Aitkenhead, 1986). When this protective mechanism is lost, cerebral perfusion pressure (CPP) becomes directly related to the systemic mean arterial blood pressure (MAP) and the intracranial pressure (ICP). Breathing patterns and fluid volumes can be manipulated in a ventilated and sedated patient. With the prescription of appropriate drug therapy, optimum blood gas levels, systemic blood pressure and, as far as possible, cerebral blood flow can be achieved, minimizing the development of additional brain damage.
The physical position and management of the patient are also important in the control of raised ICP and, in particular, the prevention of additional cerebral congestion due to obstruction of venous drainage. A slightly raised head position (avoiding neck flexion and compression of the jugular veins) is recommended (Feldman et al., 1992), although the maintenance of neutral alignment may be sufficient if raising the head threatens cerebral perfusion by lowering the systemic blood pressure (Rosner & Colley, 1986).
Activities that raise intrathoracic pressure also raise ICP and need to be minimized. This has particular relevance for respiratory care where the objective of preventing the organization of secretions must be achieved, with minimal use of interventions likely to raise ICP, such as manual hyperinflation. When a problematic chest requires vigorous attention, pretreatment sedation may be indicated, allowing bronchial suction with minimal provocation of cough. There is some evidence that slow percussive techniques may help reduce ICP (Garrad & Bullock, 1986). The principles of intervention for respiratory health are considered in detail by Ada and colleagues (1990), Roberts (2002) and in brief below (see ‘The role of the physiotherapist in the acute phase’).
Neurosurgical intervention after traumatic brain injury
In closed TBIs, surgery is undertaken as a matter of urgency to evacuate any significant haematoma and so decompress the injured brain (Jennet & Lindsay, 1994a). Where there is a depressed fracture or a penetrating wound, surgery will also be undertaken to remove any debris, clean the wound and restore the normal contour of the skull as far as possible. In some centres, minor procedures to insert an ICP-monitoring device will be performed, according to local protocols (Pickard & Czosnyka, 2000), though their use and effectiveness remains controversial (Cremer, 2008; Shafi et al., 2008; Smith, 2008).
Physical management
Beyond intervention to save life and promote the ideal conditions for cerebral repair and recovery, the next most important issue is the prevention of secondary physical changes and the provision of optimum conditions to promote physical recovery. Patients may benefit from being cared for on a special pressure-relieving mattress (Moseley, 2002) and from intensive management of nutritional input (Taylor & Fettes, 1998). Sedated patients are paralysed and vulnerable to muscular and other soft-tissue changes associated with immobility and inactivity. They are also exposed to consistent environmental stimuli, which if left unmanaged will result in significant muscle length changes. For example, the combined effects of gravity and the weight of bedding over extended periods in lying can lead to the development of foot plantarflexion.
Pathological conditions
Cerebral aneurysms
A cerebral aneurysm is an abnormal dilation or ballooning of a cerebral artery, which is usually due to a congenital or acquired weakness in the wall of the vessel (Jennet & Lindsay, 1994b). It is not usually possible to identify a single cause for the development of an aneurysm, although hypertension and arteriosclerosis are seen as risk factors. A rare form, mycotic aneurysm, results from a blood-borne infection.
Presentation
Often the first indication of the presence of an aneurysm is when it ruptures and bleeds into or around the brain. Bleeding is most commonly into the subarachnoid space (subarachnoid haemorrhage), but rupture may also result in bleeding directly into brain tissue. The incidence of subarachnoid haemorrhage in the UK is given as 10 per 100 000 population per annum (Mitchell et al., 2004), with aneurysm rupture accounting for around 75% of cases (Lindsay & Bone, 2004). Higher incidences are reported in Sweden (19 per 100 000) (Stegmayr et al., 2004) and Japan (22 per 100 000) (Ikawa et al., 2004), with a higher incidence for women reported in both studies (24% and 26% respectively). The mortality rate is reported as being between 22% (Ikawa et al., 2004) and 50% (Mitchell et al., 2004). Aneurysm rupture is most common between the ages of 40 and 60, a more mature population than the peak occurrence of TBI, but a younger age group than the mean age of 70 for stroke caused by cerebral infarct (Dombovy et al., 1998a).
Unruptured aneurysms may produce neurological symptoms due to their size or location and be diagnosed following medical investigation, including MRI brain scan. For example, a lesion on an internal carotid artery at the level of the optic chiasm can produce peripheral blurred vision (de Chigbu, 2003). Some are discovered incidentally when investigations are performed for other reasons. The diagnosis of a cerebral aneurysm is usually confirmed by angiogram, a procedure that involves injecting a radiopaque substance into the blood vessels and taking X-rays of the head (Tavernas, 1996).
Complications
Extracranial complications include cardiac arrhythmias, myocardial infarction, pulmonary oedema and stress ulcers. Hydrocephalus may occur in the early postbleed period but is also reported as a late complication in 10% of cases (Lindsay & Bone, 2004).
Medical management of aneurysms and subarachnoid haemorrhage
Subarachnoid haemorrhage is graded into five levels of severity (Table 3.5). Until the mid-1980s surgery for all grades was routinely delayed for 1–2 weeks after a bleed for fear of provoking vasospasm. However, reappraisal of the risk of a rebleed within this period and improved surgical and non-surgical techniques has encouraged more aggressive management. In most centres, intervention will be undertaken for grades I and II within 3 days (Lindsay & Bone, 2004) and in some centres early intervention is becoming routine for the majority of cases (Dombovy et al., 1998a).
Table 3.5 Grades of subarachnoid haemorrhage
| Grade | GCS | Additional descriptors |
|---|---|---|
| I | 15 | No motor deficit |
| II | 13–14 | No motor deficit |
| III | 13–14 | With motor deficit |
| IV | 7–12 | With or without motor deficit |
| V | 3–6 | With or without motor deficit |
GCS, Glasgow Coma Scale.
After Teasdale et al., 1988
Intervention for subarachnoid haemorrhage or intact aneurysms traditionally involved surgical clipping, that is, open brain surgery and the placing of a small metallic clip across the base of the aneurysm preventing blood flow into the weakened area, or embolization (Jennet & Lindsay, 1994b). Embolization is a more recent vascular technique whereby a metal coil or balloons are introduced into the artery to block off the aneurysm via the arterial system at the groin, under radiological guidance (Pile-Spellman, 1996). The choice of intervention is determined by the size and position of the aneurysm.
Physical management postintervention will vary, depending on the extent of damage caused by the prior SAH and the nature of the intervention. Endovascular treatment is usually followed by 24-hour bed rest and then mobilization. Following open surgery, management may be similar to that after surgery for TBI (see ‘Rehabilitation after brain injury’, below).
Arteriovenous malformations
A total of 40–60% of cerebral AVMs are discovered following haemorrhage, which produces symptoms such as seizures, neurological deficits or headache. Symptomatic AVMs present most frequently in the 20–40 age group and the mortality rate is lower than SAH at 10–20%. The risk of rebleed is also much less than following an aneurysmal haemorrhage and is highest for small lesions (Lindsay & Bone, 2004). Haematomas associated with AVMs are often visible on CT or MRI scans. Otherwise diagnosis will be confirmed via angiography.
Medical management of ateriovenous malformations
If and when an AVM is thought to be amenable to direct intervention, there are a number of possible options. These include surgical resection, stereotactic radiosurgery and embolization (Jennet & Lindsay, 1994b). Any one of these interventions may be regarded as the treatment of choice or, in some cases, a combination of these interventions may be used in a stepwise progression. Stereotactic radiosurgery is a method of precisely delivering radiation to a brain lesion while sparing the surrounding brain tissue (Pollock, 2002).
Infectious processes
Primary brain damage can result from meningitis, encephalitis or brain abscess.
Brain abscess
This condition is now relatively rare, with an incidence rate of 2–3 per 1000 000 population per annum (Lindsay & Bone, 2004). The infection can have its source in such things as dental caries, sinusitis, mastoiditis, subacute endocarditis or pulmonary disease.
Meningitis
Meningitis has a range of bacterial and viral sources, and a variety of presentations, associated complications and outcomes (Johnson, 1998; Kroll & Moxon, 1987). Drug therapy is commenced immediately in any suspected case, even before the infective organism is identified, and continued up to 2 weeks after pyrexia has settled.
Encephalitis
The most common form of sporadic viral encephalitis results from the herpes simplex virus which selectively affects the inferior frontotemporal lobes of the brain. This can result in extremely amnesic survivors, although treatment with acyclovir has increased survival rates to 80% and lessened resultant deficits (Lindsay & Bone, 2004).
Cerebral tumours
Primary brain tumours have an incidence level of 6 per 100 000 population with slightly less than 10% of these occurring in children (Lindsay & Bone, 2004). There are many different kinds of tumours with names reflecting the cells of origin and situation of growth. It is beyond the scope of this book to detail the treatment and prognostic factors for each kind, but it is important to note that even large tumours can be benign, resulting in a stable neurological deficit. It is clearly important to understand the nature of the tumour involved and to have the best prediction of outcome in order to structure rehabilitative intervention appropriately (see Thomas, 1990 and Al-Mefty, 1991 for further reading). The importance of developing appropriate rehabilitation and support for people with central nervous system tumours is increasingly recognized (National Institute for Health and Clinical Excellence, 2006).
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