Anxiety and Mood Disorders Following Traumatic Brain Injury

Clinical Assessment and Psychotherapy

Rudi Coetzer

• Publisher: Routledge
• Year: 2018
• eBook ISBN: 9780429910845
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

While there are many excellent texts addressing cognitive impairment and behavioural difficulties and on rehabilitation associated with traumatic brain injury, few textbooks specifically address the most common emotional problems that can have such an adverse effect on rehabilitation and outcome. Uniquely this book deals exclusively with the identification and psychotherapeutic management of mood and anxiety disorders after traumatic brain injury. Furthermore, a systematic approach to identifying and diagnosing anxiety and mood disorders is followed throughout the text. As well as providing an introduction to anxiety and mood disorders after traumatic brain injury, it provides a psychological perspective on their evolution and management. It is aimed at a range of professionals in training (or those responsible for providing training in psychopathology, neuropsychology and psychotherapy), as well as those who may have an interest in working with the type of patients with anxiety or depression, commonly seen in post-acute brain injury rehabilitation settings. Case studies, summaries and suggested references for further reading are used throughout to facilitate understanding and teaching where relevant.

Chapter One
Traumatic brain injury

Introduction

To some extent, traumatic brain injury is like the proverbial elephant in the room. In most countries of the world, the problems stemming from traumatic brain injury are well known and present significant challenges to policy makers, healthcare systems, providers of social care and clinicians. It is probably one of the most challenging healthcare problems of our time. More people today survive a traumatic brain injury than ever before, leading to an increasing demand on limited healthcare resources. While the numbers of people with traumatic brain injury may not be as enormous as some chronic illnesses for example, the problems patients experience are perhaps encapsulated in the complex and chronic difficulty following traumatic brain injury. Severe traumatic brain injury results in a wide range of impairments that almost always lead to significant disability. These impairments may be physical, cognitive, emotional, behavioural, and social, or, in many cases, a combination of these. The complex disability usually associated with traumatic brain injury does not always fit neatly into existing systems of service provision and, as a result, often pose significant challenges to providers of both health and social care.

Clearly, then, in view of the complex disability that often follows traumatic brain injury, it should become obvious to us that patients’ needs on many occasions cannot be fully met by a single provider of healthcare. As a result, patients may fall through the net and be left with extremely limited support over the long term. Traumatic brain injury and its presentation to this day continue to be poorly understood by many, including healthcare professionals. One of the potentially confusing areas is what actually constitutes a traumatic brain injury. It is important to note that not all injuries to the head necessarily result in a traumatic brain injury. Furthermore, it is important to note that this book addresses only moderate to severe traumatic brain injury. It does not address the distinctly different and complex areas encompassed by, for example, mild traumatic brain injury or post-concussion disorders. In this chapter, a brief overview of the nature of traumatic brain injury, as well as its incidence and prevalence, is provided. The reader needing access to more detailed information regarding neuro-anatomy may wish to consult a text such as that of Crossman and Neary (2000), for example.

Pathophysiology

Before proceeding to a more in-depth discussion of the pathophysiology of traumatic brain injury, it is necessary for us to consider a few general points about the topic. A traumatic brain injury does not really constitute a single, discreet event. During traumatic brain injury the brain is actually injured twice, initially as a result of physical force and subsequently because of biochemical and other changes. In view of this fact, traumatic brain injury is commonly divided into primary and secondary injuries. The primary injury is the direct result of mechanical force, meaning the actual blow to the head resulting in severe acceleration, severe deceleration, or, in some cases, both. The secondary injury to the brain results from complex biochemical changes. These follow almost immediately after the initial mechanical injury. Clearly, the direct effects of the primary injury are irreversible from the moment it happens. In contrast, some of the secondary effects can sometimes be prevented or minimized by medical or surgical intervention.

The forces applied to a person’s head during traumatic brain injury may manifest themselves differently with regard to the actual physical damage caused. Hence, at the very first level of classification or describing the damage caused by an injury, traumatic brain injuries are often classified as either an open or a closed head injury. By definition, this means that during an open head injury the brain comes into contact with the outer environment, whereas during a closed head injury it does not. Thus, in the event of an open head injury, the skull and coverings of the brain have been pierced by the injury (or the object causing the injury, for example, a hammer or bullet), thus exposing the brain. Because of this, open head injuries tend to carry a higher risk of infection than closed head injuries. Certain types of open head injuries result in more focal damage to the brain: for example, gunshot wounds or stab wounds to the head. In contrast, closed head injuries tend to result in more diffuse injury to the brain. Some of the important differences between the primary and secondary injury are discussed next.

The primary injury

As pointed out above, the primary injury to the brain is the direct result of force being applied to the head: for example, a blow to the head with an object like a hammer, cricket bat, or similar object. The substantial energy associated with these forces is transmitted to the head and then, if and when a brain injury occurs, the brain itself. This transmission of energy generally results in localized force being applied to the head or skull, as well as a sudden acceleration of the head. In other cases, the primary injury may result from the person’s head hitting a stationary or fixed object: for example, during a motor vehicle accident or a fall from a significant height. In these cases, the result is a sudden deceleration of the person’s head. Under certain conditions, both acceleration and deceleration or repeated transfer of energy can take place, such as might occur during high-speed both-end motor vehicle accidents.

In the individual case, it is, of course, not always possible to distinguish between all the different forces occurring during a head injury. In many cases, externally applied force can result in complex combinations of forces transmitted to the brain. Furthermore, under other circumstances the head is rotated suddenly, often leading to a more diffuse transmission of force. An example of this might occur when a motor vehicle travelling at high speed rolls over several times. In some cases, the transmission of force is more repeated or sustained. Although relatively rare, an example of this would be the cumulative injuries sustained over time by a boxer. However, in most cases the basic mechanisms of injury remain the same. The energy or momentum associated with these forces is ultimately transmitted to the vulnerable, soft brain tissue of the person. It should be noted, though, that injury to areas other than actual brain tissue also occurs sometimes. For example, skull fractures are common and can be divided into fractures of the skull base and the vault of the skull.

Skull base fractures do not always directly damage the brain. Some of the symptoms and signs associated with skull base fractures include, for example, loss of hearing and dizziness, or paralysis on one side of the face. These occur because of the vulnerability of certain cranial nerves, for example VII (facial paralysis) and VIII (hearing loss), being bruised or even severed as a result of skull base fractures. Furthermore, a fracture of the vault of the skull can result in an open brain injury, increasing the risk of infection of the brain tissue. Sometimes the depression in the skull associated with a skull fracture or the bone fragments themselves push on to or into the brain. This is known as a depressed skull fracture, and it should be noted that when bone fragments enter the brain, it could substantially increase the risk of the person developing post-traumatic seizures. In other cases, a skull fracture constitutes a long crack in a straight line along the surface of the skull. These are known as linear skull fractures and are perhaps not as ominous as depressed skull fractures.

Returning to the acceleration and deceleration forces typically associated with traumatic brain injury, it is important for clinicians to understand how these are transmitted inside the skull. The effects of these forces, as well as the shape of the inner bony structures of the skull, are associated with a specific and typical regional pattern of injury to the brain. Bigler (2007) provided an excellent overview of how this regional injury to the brain is related to the interface of the brain with the inner bony surfaces of the skull. The anterior poles of the frontal and temporal lobes of the brain are more vulnerable to contusions. In fact, this regional pattern of contusions is probably one of the defining characteristics of severe traumatic brain injury and leads to the rather predictable impairment of executive control function and information processing, among other cognitive difficulties. Bigler (ibid.) further pointed out that the close proximity of the hippocampus to the sphenoid ridge makes this a specifically vulnerable area in traumatic brain injury. The hippocampus forms part of the limbic system; hence, the hippocampus is of special importance because it is not only involved in memory, but, very importantly, emotion also.

It should be noted that, in many instances also, contusions are not limited to the anterior poles of the temporal and frontal lobes. Often, the brain is bounced inside the skull when force is transferred. Under these conditions, while the site of initial impact may result in predictable focal contusions, the side opposite to the blow is often severely injured also. This type of injury is known as a contre coup injury. Nevertheless, whichever way the head is accelerated or decelerated, the anterior parts of the temporal and frontal lobes are likely to be more vulnerable to injury because of the way mechanical force is transmitted throughout the brain. As a result, anosmia (loss of sense of smell) is a good clinical marker of frontal involvement after traumatic brain injury, given the proximity of cranial nerve I to the ventral aspects of the frontal lobes. The transmission of force, however, does not only affect the specific regions such as the frontal and temporal lobes. Because of the transmission of force throughout the brain, diffuse shearing and tearing of white matter (the axons of the neurons) can often take place. This is known as a diffuse axonal injury. Sustaining a diffuse axonal injury mostly results in a person being deeply unconscious immediately following injury. Diffuse axonal injury can often follow injuries resulting from severe acceleration or deceleration. An example of this is the injuries typically sustained in high-speed motor vehicle accidents.

Finally, severe traumatic brain injuries can result in bleeding, either deep inside the brain or around the coverings of the brain. Unfortunately, bleeding that occurs in the brain has nowhere to drain, because of the skull providing complete encapsulation, and hence in some cases may result in an increase in pressure inside the brain. Bleeding inside the brain is known as an intracerebral haemorrhage. These are commonly seen in the temporal and frontal lobes, but can also occur in other areas of the brain. Sometimes blood enters the ventricles. The meninges covering the brain can also be torn during severe injuries. Generally, this leads to bleeding between the skull and the outer layer of the brain (an epidural haematoma) or between the brain and the inner coverings of the brain (a subdural haematoma). Both of these complications can exert pressure effects on the brain, thus resulting in a secondary injury to the brain. Some patients require emergency neurosurgery to relieve the pressure resulting from certain types of bleeds. Bleeding inside the brain is a common example of how the primary mechanical injury resulting from traumatic brain injury can evolve into a secondary injury of the brain. Next, some other aspects of the secondary injury are briefly discussed.

The secondary injury

Perhaps the most significant difference between primary and secondary injuries to the brain is that the effect of the latter potentially can be reduced or limited in some cases by medical or surgical intervention. This is in contrast to the actual mechanical injury, where prevention is perhaps the area where healthcare professionals and policymakers should focus their efforts. Undoubtedly other areas, such as ambulance response time, airlifting casualties to hospital, and resuscitation at the scene may be a focus for improvement or development also. At the present, however, for many patients, improvements in these areas may still not be enough ever to completely avoid the risk of secondary injury in traumatic brain injury; there are, of course, also limits to the scientific knowledge base for treating traumatic brain injury during the acute phase. Many of the processes contributing to the secondary injury of the brain are not yet well understood, and more research in this area is much needed. While neurosurgical procedures have developed substantially in this area, according to Park, Bell, and Baker (2008), at this point there appear to be substantial limits to what can be achieved with pharmacological treatment of the secondary injury after traumatic brain injury.

In most cases, almost immediately after the primary (mechanical) injury, there follows a range of complex biochemical changes in the brain. For example, the levels of acetylcholine, free radicals and excitatory amino acids may rise. These and other biochemical changes can result also in reduced blood supply to the brain. Ultimately, this results in less oxygen and glucose reaching the brain tissue. As we know, brain tissue is extremely sensitive to starvation of oxygen and glucose and cannot survive for very long periods without these essential nutrients. There are also other mechanisms involved in oxygen and blood supply to the brain. Park, Bell, and Baker (ibid.) provided a comprehensive review of the biological mechanisms involved in the secondary injury after head trauma. An important factor appears to be the central role of calcium homeostasis in the secondary injury of both grey and white matter after traumatic brain injury (ibid.). This has additional relevance, as it is becoming increasingly clear that white matter damage may have significant implications for the post-acute prognosis or outcome of patients with traumatic brain injury (ibid.).

The secondary injury is, however, not only associated with biochemical changes occurring in the brain. In addition, intracerebral swelling (hydrocephalus), as well as bleeding, often take place in more severe traumatic brain injuries. These can increase intracranial pressure, thus further contributing to poor blood supply and less oxygen and nutrients reaching brain tissue. Post-traumatic cerebral infarction is relatively common: for example, Tian and colleagues (2008) reported an incidence of twelve per cent within the first two weeks following injury. Tawil, Stein, Mirvis, and Scalea (2008), on the other hand, reported an incidence of eight per cent and a significantly increased risk of mortality associated with post traumatic cerebral infarction after severe traumatic brain injury. There are also, of course, the direct pressure effects on the brain to consider. Perhaps the most dramatic evidence of the concept of a secondary injury is provided by these changes in the brain. Park, Bell, and Baker (2008) pointed out that patients who initially are able to converse after arrival at hospital, but then deteriorate and die, illustrate the point about the secondary injury being clearly separate from the primary (mechanical) injury and that it is here that future developments of treatments would most probably be focused. Finally, some of the biochemical changes associated with the secondary injury may exert a more direct negative effect by irritating the brain tissue. All these complex and interacting processes can and often do further injure the brain and have an additional adverse effect on the final outcome of the patient.

Determining severity

“How severe was the injury?” is a question we are likely to be asked many times during our careers. There are several reasons for clinicians to try to accurately assess the severity of traumatic brain injury. One of the most obvious reasons is, of course, that injury severity, along with several other factors, has a bearing on long-term outcome. While superficially appearing to be a simple process, determining with complete accuracy the actual severity of a traumatic brain injury can, in many cases, prove frustratingly difficult and challenging to even the most experienced clinicians. Many clinicians will be all too familiar with, and aware of, the dilemmas associated with determining the severity of a traumatic brain injury. This is specifically relevant in a post-acute rehabilitation setting, where ratings often have to be performed retrospectively and crucial data may not be readily available to assist with the process of determining severity. Perhaps the first task is not actually to rate severity in the first instance, but merely to determine the presence or not of a traumatic brain injury in a given patient.

What is meant by determining the presence or not of a traumatic brain injury? Not all injuries to the head result in a brain injury. Indeed, head injuries are extremely common, and most patients with a head injury make a complete recovery. It is, however, not always easy to distinguish between when a person has suffered a head injury and when a head injury actually extends to include an injury to the brain. Usually, a combination of clinical signs and findings from special investigations can be a way to confirm that a person has possibly suffered a traumatic brain injury. Traumatic brain injury is usually (but not always) associated with a period of loss or disturbance of consciousness. Post trauma amnesia tends to be a good clinical marker of traumatic brain injury also. In addition, structural abnormalities on brain imaging are common following severe traumatic brain injury. Generally, these clinical markers tend to be considered together to determine the presence and, ultimately, the severity of a traumatic brain injury.

Traditionally, the severity of traumatic brain injury has been rated as mild, moderate or severe (Guilmette, 1997), based on the Glasgow Coma Scale (Teasdale & Jennet, 1974), period of loss of consciousness, and length of post trauma amnesia, or, indeed, a combination of these markers of severity. Injuries are classified as mild where the Glasgow Coma Scale is between thirteen and fifteen, loss of consciousness is less than thirty minutes, and post trauma amnesia does not extend beyond one hour. Moderate brain injuries equate to a Glasgow Coma Scale of 9–12, and loss of consciousness between one and twenty-four hours. Traumatic brain injuries are classified as severe where the Glasgow Coma Score equals eight or less, loss of consciousness extends over a period of more than twenty-four hours, and post trauma amnesia exceeds twenty-four hours. Other forms of evidence of a traumatic brain injury include positive findings on computed tomography (CT) or magnetic resonance imaging (MRI) scans of the brain. However, we do not always have ready access to these clinical data, which can make it difficult for clinicians to determine the severity of the injury suffered by a patient.

Fortunately, Malec and colleagues (2007) provided an excellent model for overcoming the, at times, unreliability of single indicators of severity, as well as providing a clinical tool for retrospectively determining the severity of traumatic brain injury. In the Mayo Traumatic Brain Injury Severity Classification System (Malec et al., 2007), data from different sources are used in an attempt to overcome some of the significant difficulties sometimes encountered when faced with missing clinical data, for example, the absence of a Glasgow Coma Scale score or findings from neuro-imaging. Combining Glasgow Coma Scale score, post trauma amnesia, loss of consciousness, and findings from neuro-imaging, traumatic brain injury in this model is classified as moderate–severe (definite), mild (probable) or symptomatic (possible). It appears that the Mayo system correctly classifies more cases of traumatic brain injury as opposed to when a single indicator of potential severity, for example, neuro-imaging, is used.

Neuro-imaging

Brain imaging is not only used to determine severity. The development and also wider availability of high quality anatomical imaging, for example, CT and MRI scans of the brain, has, without any doubt, more generally contributed immensely to the acute and post-acute care of patients with traumatic brain injury. In many cases, findings from scans reveal the tell-tale pattern of contusions and other abnormalities classically associated with traumatic brain injury, ensuring diagnostic accuracy. As an illustration, a person might make a complete physical recovery after a traumatic brain injury, but present with behavioural or emotional difficulties, which can be interpreted as “being difficult”, until appropriate imaging may suggest a link to the injury, thus ensuring appropriate treatment or rehabilitation. Nevertheless, in many cases scans are normal. These findings, however, should be interpreted with caution, especially during the very early stages following injury. Scan results can change over time. In this regard, Bigler (2001) warned that the absence of positive findings on CT or MRI does not necessarily always rule out the presen...

Table of contents

• Cover
• Half Title
• Title
• Copyright
• Contents
• ACKNOWLEDGEMENTS
• ABOUT THE AUTHOR
• Dedication
• SERIES EDITOR'S FOREWORD
• PREFACE
• CHAPTER ONE Traumatic brain injury
• CHAPTER TWO Clinical presentation
• CHAPTER THREE Assessment
• CHAPTER FOUR Psychological approaches to the management of anxiety and mood disorders
• CHAPTER FIVE Panic disorder
• CHAPTER SIX Phobias
• CHAPTER SEVEN Obsessive-compulsive disorder
• CHAPTER EIGHT Post traumatic stress disorder
• CHAPTER NINE Generalized anxiety disorder
• CHAPTER TEN Major depressive disorder
• CHAPTER ELEVEN Bipolar disorder
• CHAPTER TWELVE Special populations
• CHAPTER THIRTEEN Conclusions and future directions
• REFERENCES
• INDEX