Published on March 4, 2014
NEUROSURGERY The fundamentals of head injury Epidemiology and aetiology Trauma is the leading cause of death of young people (<40 years) in the Western world. Approximately 40% of patients with serious polytrauma have sustained a head injury. The overall incidence of head injury is difﬁcult to ascertain, however it is estimated to be 400 per 100,000/year or roughly 1.4 million per year in the UK alone. Of these, around 10% are classiﬁed as moderate or severe. Care for these patients is expensive. Once out of the acute setting, patients continue to need long periods of support and, because of the nature of their cognitive deﬁcits, many never return to their previous lives. Hence traumatic brain injury (TBI) is costly both in terms of the resources needed to treat patients and in the toll exacted on the patient’s quality of life. David Baxter Mark Wilson Abstract In the Western world, trauma is the commonest cause of death in the under-40s, and, head injury is the leading component of this. Traumatic brain injury (TBI) is not a single disease, but a number of pathologies that can occur in isolation (e.g. an extradural haematoma) or co-exist (a subdural haematoma with diffuse axonal injury). TBI has important social, emotional and ﬁnancial consequences, both for the individual, their families and society. Despite this, there is a great deal we do not know about brain injuries and how best to manage them. This article outlines the fundamental principles of pathophysiology, diagnosis and management. Mechanisms of injury In the UK blunt injuries are the most common type of head injury with motor vehicle accidents, falls and assaults being the commonest causes (in that order). In the USA, the commonest cause of TBI related death is ﬁrearms. This is comparatively rare in Europe. Blast injuries, whilst rare in civilian peacetime, are common in the military setting and terrorist or explosion related major incidents. Keywords Burr hole; head injury; intracranial pressure; neurotrauma; trauma craniotomy; traumatic brain injury Pathology and pathogenesis Primary vs secondary injury Primary brain injury is the injury sustained at the time of impact. Public health measures prevent primary injuries, but medical management can do little to reverse them. Secondary brain injury is any injury that occurs after the primary and hence should be preventable or at least treatable. Sadly they often account for much of survivors’ ﬁnal brain injury. For example, an extradural usually has no underlying brain injury, however the accumulating blood can increase pressure on the brain and eventually cause death e all from a treatable secondary brain injury. There are a number of types of secondary injury, for example: hypoxia from an obstructed airway; ischaemia from poor cerebral perfusion (e.g. due to hypovolaemia); raised intracranial pressure and reduced perfusion (from accumulation of intracranial haematoma or oedema). On a cellular level, a cytotoxic cascade initiated by calcium inﬂux due to the presence of glutamate can occur. Very severe brain injuries can result in neuronal breakdown triggering a devastating inﬂammatory response with disseminated intravascular coagulopathy. Good pre-hospital care optimally managing the patient’s injuries while rapidly transporting them to an appropriate centre is essential for the prevention and reduction of secondary brain injuries. Quicker surgical intervention to reduce brain insult results in a better outcome. Class III evidence shows that where time from injury to surgery exceeds 2 hours, the mortality rate for patients with extra- or (acute) subdurals nearly doubles. Deﬁnition and classiﬁcation The term ‘head injury’ is often used interchangeably with the term ‘brain injury’ or ‘traumatic brain injury’ and refers to an injury to the brain or skull acquired through traumatic means (as opposed to a non-traumatic brain injury acquired secondarily to, for example, a stroke or cerebral abscess). Injuries to the face are Maxillofacial injuries and are not discussed in this article. Traumatic brain injuries can be classiﬁed in a number of ways e for example, by mechanism (blunt/penetrating), by level of consciousness (mild, moderate or severe)1 or radiologically (Marshall classiﬁcation).2 Unfortunately, these systems are not ideal. They poorly predict outcome and give the false impression that ‘brain injury’ is a single disease. It is vital that over the next decade, a better classiﬁcation system is developed. This will enable better study and prediction of outcome.3 Separately, skull fractures can be classiﬁed as vault or base of skull fractures. These can be open or closed, undisplaced or (uniquely for skull fractures) depressed. David Baxter BSc MBBS is an Army Neurosurgical Specialist Registrar and Research Fellow at Imperial Hospitals NHS Trust and Imperial College, London, UK. Conﬂicts of interest: none declared. Mark Wilson BSc MBBChir FRCS (SN) FIMC FRGS MRCA is a Consultant Neurosurgeon and Honorary Senior Lecturer at Imperial Hospitals NHS Trust and Specialist in Pre-Hospital Care with London’s Air Ambulance (HEMS), Barts and the London NHS Trust, UK. Conﬂicts of interest: none declared. SURGERY 30:3 Gross pathology Blunt injuries Blunt injuries can result in a number of pathologies (and often a combination). The extra-axial haematomas (extradural and 116 Ó 2012 Elsevier Ltd. All rights reserved.
NEUROSURGERY Diffuse axonal injury The same blunt forces (and especially rotational forces) can also disrupt the white matter ﬁbre tracts within the brain. This is more difﬁcult to appreciate on CT, but can be seen on certain MRI (susceptibility weighted) scans. Areas commonly affected include the corpus callosum and brainstem and, depending on severity, can result in conditions from mild concussion to a persistent vegetative state. With blunt injuries, there is often some traumatic subarachnoid blood visible on CT. This does not usually require any speciﬁc intervention. subdural haematomas) are explained in Figure 4 page 114, with a brief review here. Extradural haematoma: an extradural haematoma is classically caused by a direct blow over the temporal region resulting in a fracture and middle meningeal artery injury. This strips the dura from the inner surface of the skull (giving a convex or egg shaped appearance, Figure 1). Subdural haematoma: a subdural haematoma is classically caused by shearing of the brain from the inside of the dura. Small bridging veins are put under tension causing them to bleed. The accumulating venous blood is not bound by any dural attachments to the skull and spreads across the brain’s convexity. Subdurals can be acute (dense/white on CT), which is common in young people after severe rotational injuries, or chronic (hypodense/dark), which tend to occur in older folk who have a slow accumulation of blood following a minor knock. Penetrating injuries: occasionally, blunt mechanisms can result in open injuries. For example, a compound depressed skull fracture where bone fragments have penetrated the dura. Usually however, open injuries are a result of penetrating trauma (missiles such as bullets, shrapnel or implements such as knives or tools). Such injuries can directly disrupt neuronal tracts and, if they involve major blood vessels, can result in catastrophic injury. However, if the patient survives, it is usually the problems of infection or epilepsy (from focal neurological injury) that are the most pressing. Contusions and haematomas: in blunt (or closed) head injury, the primary damage occurs because of sudden changes in forces or direction of these forces. These can be deceleration/acceleration and/or rotational forces. If the head is travelling at speed and suddenly decelerates, the brain will continue to travel inside the skull and damage occurs as it impacts bony contours inside the skull. This results in a ‘coup’ injury. Contusions opposite the site of impact are called ‘contre-coup’. These contusions (bruises) are also common where the brain is sheared across the rough base of skull surfaces, the anterior and temporal fossa being classic locations. If a contusion coalesces, it is said to form an intraparenchymal (within the brain) haematoma. a Extradural Intracranial pressure Intracranial pressure (ICP) is the pressure within the cranium. Because the skull acts as a closed box, the addition of another volume (e.g. an expanding haematoma) requires the reduction of a compensatory volume (cerebrospinal ﬂuid (CSF) or venous blood). Once this compliance is at its limit, any additional volume results in a rise in intracranial pressure. This phenomenon is known as the MonroeKellie doctrine (Figure 2a). b Subdural Hypodense blood (older) on top of (hyperdense) blood. Hence this is not an acute subdural Minimal midline shift as in this case older (more atrophic brain) affords more compliance Lateral ventricle effaced Lenticular hyperdense (acute blood) collection Fracture Overlying swelling Midline shift Effacement of right lateral ventricle The shape of the collection results from dura ‘sticking’ to the inside of the skull c Shape results from no restrictions to blood over surface of brain d Contusions Diffuse axonal injury (seen better on delayed (that have evolved to form bifrontal haematomas) magnetic resonance imaging) Petechial haemorrhages Poor grey-white differentiation General appearance of being ‘tight’ Figure 1 Composite of computed tomography images demonstrating (a) an extradural haematoma, (b) a subdural haematoma, (c) contusions and (d) diffuse axonal injury. (Adapted with permission from Head Injuries, The Oxford Desk Reference of Trauma, Ed Smith, Greeves and Porter, Oxford Press, 2010). SURGERY 30:3 117 Ó 2012 Elsevier Ltd. All rights reserved.
NEUROSURGERY a b Compliant brain Intracranial pressure Tight brain Increasing cerebral blood volume or oedema Figure 2 (a) The MonroeKellie doctrine. An expanding mass or increase in volume within the cranium results in a compensatory expulsion of cerebrospinal ﬂuid and venous blood. When at its limits, this compliant system changes to a hydraulic system resulting in a rapid rise in ICP (from Wilson et al 20094). (b) The different brain shifts and coning. (1) Subfalcine herniation, (2) transtentorial herniation, (3) uncal herniation (as the medial aspect of the temporal lobe is forced around the tentorium by an expanding temporal haematoma, pressure on the oculomotor nerve will result in unopposed sympathetic pupil activity (pupil dilatation) and (4) tonsillar herniation. (Adapted with permission from Head Injuries, The Oxford Desk Reference of Trauma, Ed Smith, Greeves and Porter, Oxford Press, 2010). A rise in ICP can result in brain shifts and coning (Figure 2b). The classic teaching of head injury management is that CPP must be maintained to ensure adequate blood supply to the brain. However, the ‘ideal’ CCP is not known. To maintain CPP, either the mean arterial pressure (MAP) can be raised or the ICP lowered (always aim to lower ICP ﬁrst). The partial pressure of CO2 also has dramatic effects on CBF. Hyperventilation (voluntarily by the patient or by an over enthusiastic paramedic/anaesthetist) results in pCO2 falling and vasoconstriction. This reduces ICP, but also reduces cerebral perfusion. Hypoventilation (e.g. from an obstructed airway) results in a rise in pCO2 and an increase in cerebral blood ﬂow. However, it also results in a rise in ICP, so current guidelines state to aim for normal end tidal CO2 (approximately 4.5 kPa). Cerebral blood ﬂow Cerebral blood ﬂow (CBF) can be affected by a number of factors, however, arterial blood pressure, ICP and carbon dioxide (CO2) tensions are those that are particularly important in head injury. The normal autoregulatory processes that maintain a consistent cerebral blood ﬂow are said to be lost in severe head injury (Figure 3). Cerebral perfusion pressure (CPP) is regarded as the driving arterial pressure at the point of entry into the brain. In someone supine, this can be considered the balance between the blood pressure driving blood in and the intracranial pressure forcing blood out. Hence: CPP ¼ MAP À ICP ðe:g: 75 mmHg ¼ 90 mmHg À 15 mmHgÞ Effects of arterial blood pressure, the partial pressure of carbon dioxide (PaCO2) and the partial pressure of oxygen (PaO2) on cerebral blood flow (CBF) b 100 80 Cross-section of cerebral arteriole Cerebral blood flow (mL/100 g/minute) Cerebral blood flow (mL/100 g/minute) a 60 40 20 Autoregulation 0 0 3 6 PaCO2 (kPa) 9 0 12 50 100 150 Cerebral perfusion pressure (mmHg) 200 (Reproduced from Gardiner et al Training in Surgery 2009, Oxford University Press). Figure 3 SURGERY 30:3 118 Ó 2012 Elsevier Ltd. All rights reserved.
NEUROSURGERY Burr holes and trauma craniotomy Location of burr holes ‘Trauma flap’ Zygomatic arch 3 2 1 1 cm (Adapted from Head Injuries, The Oxford Desk Reference of Trauma, Ed Smith, Greeves, and Porter, Oxford Press, 2010). Figure 4 Cellular pathology bleeding or cerebrospinal ﬂuid from the ears (otorrhoea) or nose (rhinorrhoea). Other base of skull fracture signs include bilateral bruising behind the ears (Battle’s sign) and bruising under the eyes (panda/racoon eyes). Pupillary examination should be carried out in all patients with a reduced level of consciousness. A dilated pupil may signify an expanding haematoma causing pressure on the ipsilateral oculomotor nerve. The patient needs to be packaged and transported to the appropriate centre (with neurosurgical expertize). In a trauma setting, head injury should be presumed until shown otherwise in a patient with a reduced level of consciousness. Examination of the patient’s consciousness level is therefore key in diagnosing head injury, and is usually carried out by one of two methods: Glasgow Coma Scale (GCS) and AVPU. The Glasgow Coma Scale (GCS, Table 1) is a 15-point system for repeatable monitoring of a patient’s ‘level’ of consciousness. The response of the eyes, voice and motor capacity of the patient are assessed with the scores added together, the lowest achievable score being 3. GCS is used as a marker of the severity of head injury: mild ¼ 14e15; moderate ¼ 9e13; and severe ¼ 3e8. It is the standard classiﬁcation system used in head injury because it is easy to perform and reproducible between different healthcare professionals. The motor score is thought to have a stronger weighting than eye or voice scores and so a breakdown of the scores is essential when discussing patients. There are a number of brain injury models. One model for focal injuries divides brain into an injured (and permanently damaged) central area, with a surrounding area of ‘salvageable’ penumbra which in turn is surrounded by an area of normal brain. This may not be applicable to all injuries, but it highlights that in some areas, the metabolic status of neurons and surrounding cells is on edge. Ischaemic neurons release glutamate which triggers a cytotoxic cascade of calcium inﬂux and further glutamate release. Many pharmacological interventions have been tried to prevent this cytotoxic cascade, but as yet, none have achieved clinical use. Diagnosis and initial management (Current UK Guidelines can be found within the National Institute for Health and Clinical Excellence (NICE) head injury guidelines http://www.nice.org.uk/CG56). Basic head injury care must be carried out simultaneously with assessment to minimize secondary injury. This includes: Airway (with c-spine control): this may mean intubation if the patient has a reduced level of consciousness or is unable to protect their own airway. Oxygen should always be administered. Breathing: if intubated, aim for normocapnia (EtCO2 of 4.5 kPa). Circulation: try to minimize hypotension (reduce/splint fractures, direct pressure/elevate/tourniquet actively bleeding wounds). AVPU is an acronym popularized by Advanced Trauma Life Support training. It involves an assessment of the patient as Alert, responding to Voice or Pain, or being Unresponsive. These have been shown to correspond to median GCS scores of 15, 13, 8 and less than 6, respectively. AVPU is a simpler system to GCS but less sensitive to change. Disability: assess as detailed below. Exposure: examination of the head for lacerations, bruising or foreign bodies. A base of skull fracture can be indicated through SURGERY 30:3 119 Ó 2012 Elsevier Ltd. All rights reserved.
NEUROSURGERY Cooling patients to 35 C reduces ICP. Further research is necessary to determine whether mild hypothermia also offers neuroprotection in head injury. Adult and paediatric Glasgow Coma Scale Eye opening (E) Spontaneous To voice To pain None Verbal response (V) Orientated Confused conversation Inappropriate words Incomprehensible sounds None Motor response (M) Obeys commands (normal movement in children) Localizes pain Normal ﬂexion (withdrawal) Abnormal ﬂexion (decorticate) Extension (decerebrate) None (ﬂaccid) Paediatric verbal response (V) Best response for age (as before injury) Confused or spontaneous irritable cries Cries to pain Moans to pain None 4 3 2 1 Non-depolarizing muscle relaxants reduce ICP and reduce the body’s overall metabolic requirements. They are especially useful if a patient is being cooled where the relaxants prevent shivering, which can raise ICP. 5 4 3 2 1 Maintenance of glucose within the normal range prevents hypo and hyperglycaemic induced neuronal necrosis. Caloric and nitrogen provision is required as patients with severe brain injuries have metabolic responses similar to patients with 20e40% surface burns. 6 Anti-seizure medication helps prevent seizures that can increase ICP and metabolic demand. Phenytoin can be used for 1 week following moderate/severe head injury in order to prevent damage caused by seizure. In most circumstances (if there have been no seizures) they should be stopped after 1 week as there is no evidence they prevent development of late-onset seizures. 5 4 3 2 1 5 4 3 2 1 Antibiotics in accordance with the department’s protocol should be prescribed for compound skull fractures. These injuries should be debrided and closed surgically (with the exception of fractures which cross a major venous sinus where the risks of surgery outweigh the beneﬁt). Patients with base of skull fractures and CSF leakage should not routinely be given antibiotic prophylaxis, as they will often not require treatment and antibiotics may predispose the patient to resistant bacteria. These patients must be observed in the hospital setting until the leak stops as there is a risk of meningitis while leaking. Steroids have been trialled in traumatic brain and spinal cord injury as a means of reducing oedema. In 2004, the CRASH study5 was terminated early because of an increased mortality associated with steroid use. Steroids are not used in head injury management. Barbiturates reduce the cerebral metabolic rate and ICP, and they have been shown to be protective in cerebral anoxia and ischaemia. However, as with sedatives, barbiturates have the effect of also reducing blood pressure and their use in hypotensive patients has been correlated with a worse outcome. Induction of a barbiturate coma is therefore the last step in medical management of refractory raised ICP. Studies to date have failed to show any beneﬁt from the use of nimodipine, magnesium or free radical scavengers in medical management of traumatic brain injury. Table 1 The combative patient: patients with a head injury may be combative. It is often difﬁcult to establish if drugs/alcohol/their personality is causing such aggression. If not appropriate, they are not GCS 15. Although alcohol is involved in many head injuries, it is safest to assume that any altered level of consciousness is due the head injury. Paediatric GCS: the assessment of children with head injuries can be exceptionally difﬁcult. The verbal component is assessed differently (Table 1). The deﬁnitive diagnosis of brain injury in a patient with a reduced level of consciousness is usually by CT scan. Medical management There are a variety of non-invasive measures that can be used to reduce ICP. The patient should be nursed with the head end of the bed tilted 30 up to allow better drainage of the jugular venous system. Care must be taken to check an ill-ﬁtting cervical collar does not constrict the neck. Surgical management The aim of most surgical management of head injury is to reduce ICP either by removing a mass lesion (e.g. haematoma) or by removing part of the skull to provide larger areas for the brain to expand into. Diuretics such as mannitol can be used to temporarily reduce ICP to ‘buy time’ when surgery is imminent. Hypertonic saline can also be used in a similar manner. It may well be preferable especially in the hypovolaemic patient, and it has a more sustained effect. Intracranial pressure monitoring The insertion of an ICP monitor (‘bolt’) is a surgical procedure that allows medical and surgical decision-making in order to control ICP. The bolt is normally inserted ipsilateral to the injury (or on the non-dominant side) in the mid pupillary line, 10 cm Sedation is used to help control ICP medically through reducing agitation and lowering the metabolic rate of the brain tissue. SURGERY 30:3 120 Ó 2012 Elsevier Ltd. All rights reserved.
NEUROSURGERY behind the eye (Kocher’s point). A pressure transducer is then passed into the parenchyma of the brain before being ﬁxed in place to a bolt screwed into the skull. A rapid rise in ICP in a patient with a known intracranial bleed may represent further bleeding and requires repeat scanning with a view to evacuation of the blood. Prevention of disease/condition Ventricular drainage Prognosis and explanation to patient Ventricular drainage can be used to monitor ICP as well as to treat by removal of CSF from the ventricular system. A rise in ICP can result in effacement of the lateral ventricles and displacement of CSF. This procedure carries the risk of a haematoma formation during insertion of the catheter, seizures and subsequent infection of the CSF. Outcome from head injury is very difﬁcult to predict in the acute setting, and outcome can vary widely. The patient should have a detailed neuropsychological assessment that examines processing speed, memory, concentration and insight. The latter is particularly important as patients who lack insight do not fully appreciate the level of their injury and ﬁnd it difﬁcult to develop coping strategies. To date, the greatest improvement by far in the management of head injury has come from preventative strategies, such as helmets, seatbelts and trafﬁc safety measures. Possible strategies in the future will revolve around alcohol legislation, prevention of falls in the elderly and military body armour improvements. Haematoma evacuation The future Evacuation of haematoma is usually appropriate for patients with a high ICP and a surgically accessible lesion. The surgical technique used depends on the nature and location of the clot (Figure 4). For chronic subdurals (or to quickly relieve a raised ICP from an extradural before proceeding to craniotomy), one or two burr holes in the appropriate locations may be performed. For a temporal extradural or acute subdural, a convexity craniotomy through a questionmark ‘trauma’ incision would be a standard approach. Head injury is still poorly understood and devastating. Lessening its impact will require a multi-pronged approach, with prevention and investment in rehabilitation taking a lead. In the acute setting, improvement of trauma systems will allow head injured patients to be treated promptly at the appropriate centre. A REFERENCES 1 Jennett B, Teasdale G. Aspects of coma after severe head injury. Lancet 1977; 1: 878e81. 2 Marshall LF, Marshall SB, Klauber MR, et al. The diagnosis of head injury requires a classiﬁcation based on computed axial tomography. J Neurotrauma 1992; 9(suppl 1): S287e92. 3 Saatman KE, Duhaime AC, Bullock R, Maas AI, Valadka A, Manley GT. Classiﬁcation of traumatic brain injury for targeted therapies. J Neurotrauma 2008; 25: 719e38. 4 Wilson MH, Newman S, Imray CH. The cerebral effects of ascent to high altitudes. Lancet Neurol 2009; 8: 175e91. 5 Roberts I. The CRASH trial: the ﬁrst large-scale, randomised, controlled trial in head injury. Crit Care 2001; 5: 292e3. 6 Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011; 364: 1493e502. Decompressive craniectomy Decompressive craniectomy involves removing a large part of the cranium to allow the underlying swollen brain to expand out of the constraints of the skull, resulting in a reduction in ICP. This is a complex procedure and, to date, there is insufﬁcient evidence of its long-term beneﬁt. A recent trial6 (which investigated the use of decompression at an ICP of 20 mmHg) found a worse outcome with surgery. Rescue ICP is an on-going study that should report in a couple of years. Outcome following TBI/rehabilitation The Glasgow Outcome Score (GOS) originally described outcomes as falling into ﬁve categories: death, persistent vegetative state, severe disability, moderate disability and good recovery. Persistent vegetative state refers to the inability to communicate or follow commands. Severe disability refers to conscious patients who require assistance with basic needs such as feeding and hygiene. Moderate disability means some persistent neurologic or cognitive impairment but can manage basic needs, use public transport and work in a sheltered situation. To increase sensitivity, the severe and moderate disability and good recovery outcomes have been divided into upper and lower categories and so the revised GOS has an eight-point rather than a ﬁve-point scale. Patients classically complain of problems of concentration, memory, emotional labiality, difﬁculty sleeping, and impaired processing speed. In addition to this, the anterior pituitary gland, because of its vulnerable position in the skull, is injured in 15e 50% of cases of traumatic brain injury and produces deﬁciencies in cortisol and growth hormone. SURGERY 30:3 FURTHER READING BOOKS New York. In: Valadka, Thieme Andrews, eds. Neurotrauma e evidence based answers to common questions 2005. EDITORIAL Neuroanaesthesia and Neurocritical Care Postgraduate Educational Issue of British Journal of Anaesthesia. Vol 99 Number 1 July 2007. RELEVANT GUIDELINES Brain Trauma Foundation Guidelines for prehospital, surgical, combat related management of head injuries: http://www.braintrauma.org. Cochrane Reviews for evidence based management: http://www.cochrane.org. NICE Head Injury Guidelines: http://www.nice.org.uk/guidance/cg56. 121 Ó 2012 Elsevier Ltd. All rights reserved.
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