Headaches and Brain Injury from a Biopsychosocial Perspective

A Practical Psychotherapy Guide

Birgit Gurr

• Publisher: Routledge
• Year: 2018
• Print ISBN: 9781782201014, 9780367102531
• eBook ISBN: 9780429914447
• Edition: 1
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

Post-traumatic headache is the most common symptom after mild/moderate brain injury. Similar to the characteristics of naturally occurring headaches, it is multi-faceted in nature and includes neurophysiological, psychological and social aspects. Consequently, headache has an enormous impact on the quality of life of the sufferer. Effective headache treatment has a focus on all aspects of the pain and the needs of the individual. This book describes a cognitive-behavioural program which was developed as part of a research project in a brain injury service. It is based, firstly, on the evidence provided by the outcomes of this research project. The interested reader may study the literature associated with this research for which the references can be found at the back of this volume. Secondly, this headache therapy guide is the result of clinical experience and the application of cognitive behavioural therapy to patients who experience complex difficulties following a brain injury.

PART I

THEORY

CHAPTER ONE

Headaches and brain injury

Clinicians and researchers have long been puzzled by patients presenting with enduring problems following brain injury. Literature on mild brain injury, post-concussion symptoms, and post traumatic headaches frequently reports the lack of symptom specificity, the controversies and complexities surrounding the existence of such problems, and the rarity of good studies helping to identify their causes and consequences. Consequently, doctors and therapists have often felt paralysed in their attempts to offer helpful treatments for headache patients.

This chapter attempts to present the available knowledge about headaches and brain injury in a structured way. By showing that an understanding of the condition and its psychological treatment is possible, despite weaknesses in medical or scientific descriptions, scaffolding for later sections of the book will be provided.

Brain injury or head injury?

The terms “brain injury” and “head injury” are used in the literature almost synonymously and, while they are closely related, it is useful to distinguish between them. The term “brain injury” describes a condition associated with changes within the brain, usually assumed to have been preceded by some sort of external trauma, or “head injury”.

This book focuses on patients who have sustained a brain injury and, therefore, possibly injuries to structures of the head and the mechanisms of the brain. Mild traumatic brain injury is associated with concussion. Concussion and post-concussion syndrome describe the sort of difficulties associated with mild brain injury.

The scale and severity of the problem

Brain injuries due to accidents are a major health problem. Over 100,000 adults are discharged from UK hospitals with a diagnosis of traumatic brain injury each year. Based on rates of people presenting to Accident and Emergency Departments, the annual incidence of head injuries is said to be around 250 to 300 per 100,000 in the general population (Allen, 2007). Motor traffic accidents are the most frequent causes; others include physical assaults and sports injuries. Young males are most at risk, especially if there are co-existing factors such as alcohol or drug abuse, psychiatric history, or low socio-economic status. Older adults are more vulnerable to brain injury due to the increased risk of falling (Packard, 1999).

The severity of traumatic brain injury is typically described as mild, moderate, or severe. A mild traumatic brain injury is classified as a traumatically induced loss or alteration of consciousness lasting less than thirty minutes or a period of post traumatic amnesia lasting less than twenty-four hours or resulting in a Glasgow Coma Scale (GCS) score of 13–15 (Teasdale & Jennett, 1974). Moderate traumatic brain injury involves loss of consciousness between thirty minutes and twenty-four hours, GCS score of 9 to 12, or length of post traumatic amnesia between one and seven days. Severe traumatic brain injury involves periods of coma and post traumatic amnesia beyond the timeframe for moderate injury (Cuccurullo, 2004).

Post-concussion syndrome

In the case of a brain injury classified as mild or moderate, patients may experience a range of disabling problems described as postconcussion syndrome. The core symptoms of this condition are:

• physical: headache, fatigue, dizziness, sensitivity to light and noise;

• emotional: irritability, anxiety, depression, anger, stress;

• cognitive: concentration and memory problems, reduced mental speed;

• other: lower tolerance of alcohol, insomnia, tinnitus, preoccupation with brain injury.

Symptoms may develop within a two-week period following the injury and are normally expected to resolve within three months. Nevertheless, many patients experience persistent problems beyond this time period. Psychological factors, especially anxiety, poor motivation, and inappropriate coping strategies, can play a significant role in the maintenance of such symptoms. Further risk factors for the development of post-concussion symptoms include psychological or psychiatric presentations (premorbid and comorbid), alcohol or substance misuse, and the pursuit of compensation claims (Hou et al., 2012).

The organic component of concussion is caused by the rotation or deceleration forces that lead to mechanical injury or deformation of the neural tissue. Diffuse axonal injury, associated with the tearing, stretching, compressing, or shearing of axons and the swelling of brain tissue are very common structural changes in concussion. Metabolic and neurophysiological changes ultimately contribute to the physiological vulnerability generated by this condition. It is, therefore, not surprising that people with enduring concussion symptoms experience information-processing difficulties, which are essentially caused by disturbances of neurotransmitter flow, the processing of chemical messages and their conversion into electrical potentials. The brain-injured person may become aware of these abnormalities in the form of cognitive under-performance, particularly in the areas of attention, short-term memory, mental speed and flexibility.

Headaches following brain injury

Headaches are associated with minor or moderate brain injuries. They are also called post traumatic headaches to mark their distinction from idiopathic headaches such as tension headaches or migraines.

Headaches following a brain injury are understood within the context of the post-concussion syndrome. Headaches after brain injury have, like the post-concussion syndrome, a multi-faceted aetiology caused by organic impairment and influenced by psycho-social attributes. The incidence of headaches after brain injury is as high as 90%, so it is almost a universal symptom and definitely the most common symptom after mild brain injury (Martelli, Grayson, & Zasler, 1999; Saper, 2000; Wood, 2004). This suggests that the rehabilitation of headaches after brain injury can facilitate the recovery from concussion.

Couch and Bearss (2001), and also Zasler (2012), showed an inverse relation between the extent of a brain injury and the occurrence of chronic daily headaches. Seventy-three per cent of patients with minimal brain injury suffered chronic daily headache, whereas only 27% of patients with moderate/severe brain injury had chronic daily headache. How can this be explained? It is assumed that people who survive severe brain injury are initially immobilised due to the injury and efficiently medicated. This optimal rest period means that the body has an opportunity to rebalance its mechanisms as part of natural healing. Coma and post traumatic amnesia interfere with the patient’s ability to remember and reflect on the psychologically traumatic impact of the accident. Reduced awareness further limits the development of central sensitisation processes (see below). Nevertheless, clinicians and researchers have become aware of a substantial number of patients with moderate to severe brain injury who experience persistent headaches (Gurr & Coetzer, 2005; Horn, Siebert, Patel, & Zasler, 2013).

Premorbid headaches and previous concussion episodes generate a vulnerability for headaches following brain injury (Zasler, 2012). A genetic predisposition to headaches may not only pose a risk, but may worsen the outcome (Gennarelli, 1993). Women are reported to suffer headaches more frequently after brain injury than men (Jensen & Nielsen, 1990). Age and low socio-economic status also seem to have a negative effect on recovery (Bohnen, Twijnstra, & Jolles, 1992; Faux & Sheedy, 2008). Dawn (2003), in his comparative study, found that patients with brain injury reported higher headache frequency and disability than patients with idiopathic headache.

Most improvement of headaches is expected during the first three to six months following the injury. Beyond that time, there is a greater tendency for the symptoms to become chronic. Packard and Ham (1994) report a persistence of headaches after brain injury for more than three years in 15–30% of cases. Martelli, Grayson, and Zasler (1999) report an incidence of brain injury-related headaches persisting longer than six months as high as 44%; cases lasting around four years were estimated to be about 20%.

Headache diagnosis and classification

Headaches are diagnosed as either primary or secondary headaches. Primary headaches are not associated with a particular underlying disease and are also called idiopathic headaches. Headache after brain injury is a secondary type and is classified by the International Headache Society (2013) into acute and chronic post traumatic headache. The criteria for acute post traumatic headache require that the headache begins seven days after the injury and disappears three months following the injury. Chronic post traumatic headache is classified for headaches persisting beyond three months. Headache after brain injury can be differentiated according to injury severity, whiplash, surgical craniotomy, traumatic intracranial haematoma, other head or neck trauma, and pre-existing headaches. The criteria of the International Headache Society allow coding for more than one type of headache in a patient.

The diagnosis and treatment of headaches after brain injury can be difficult as they involve subjective symptoms with unclear evidence of organic abnormality. Genetic, biological, and psychological predisposing factors play a role in the genesis and maintenance of the problem (Packard, 1999; Packard & Ham, 1994).

The diagnostic description is further complicated by the difficulty of accurately identifying reliable neurometabolic biomarkers. Advanced developments in technology, such as proton magnetic resonance spectroscopy (Vagnozzi et al., 2010; Yeo et al., 2011) might provide a better means of assessing mild brain injury in future, as neurophysiological changes could be detected.

Specific types of headaches following brain injury

Individuals who have experienced a brain injury may develop one or several types of headache. The most common presentations, tension headache, migraine, cluster headache, and mixed post traumatic headache, are clinically similar to their non-traumatic counterparts.

Tension headache

This is a very common headache type following brain injury. It is regarded as a muscular tension and associated with musculoskeletal problems in the neck. Tension headache may be chronic or episodic. Stress appears to be a highly related factor. Combinations of tension type and vascular headache are possible. Radanov, Di Stefano, and Augustiny (2001) argue that pre-traumatic headache provides a risk factor for the development of headaches after brain injury on the basis of pre-existing central sensitisation, triggered by muscle contractions at the time of injury and confounded by a psycho-social predisposition. Although migraine after brain injury seems extensively described in the literature, it appears that tension headache is more common (Haas, 1996; Zasler, 2012).

Migraine

The clinical features of migraine after brain injury are almost identical to those of idiopathic migraines, either with or without aura. Their characteristics include migraine attacks with throbbing, lateralised headache accompanied by nausea, vomiting, photophobia, and response to classic migraine medication (Goldstein, 1991). Maladaptive neurophysiological activation causes the release of pain-producing inflammatory substances around the nerves and blood vessels of the brain. It is postulated that a latent genetic predisposition to migraine is triggered following a brain injury (Weiss, Stern, & Goldberg, 1991). Consequently, injury-related migraine would be normal migraine occurring after a brain injury (Packard & Ham, 1994). Preexisting migraine can be exacerbated following trauma to the brain. There seem to be neurochemical mechanisms in migraine that overlap with changes that occur in mild brain injuries. These similarities may play an aetiological role in some headache problems that occur after an injury (Packard & Ham, 1997, see below).

Cluster headache

This is a more unusual headache syndrome following brain injury that, as the name implies, occurs in episodic clusters (Packard & Ham, 1996). The onset of this type of vascular headache is usually very fast with a relatively short duration.

Direct and injury-related headaches

Medical causes for headaches which can be directly related to the injury include cerebral vein and sinus thrombosis, subdural and epidural haematoma, intracerebral and subarachnoid haemorrhage, altered intracranial pressure, hydrocephalus, carotid and vertebral artery dissection, cavernous–carotid fistula, cerebral aneurysms, skull and cerebral vertebrae fracture, and cervical disc protrusion.

Other types of headache

Cervicogenic headache is very common following brain injury. This is due to the force of the blow to the head also affecting the musculoskeletal regions of the neck and upper spine. In a typical car accident, the head bends rapidly backwards, causing the mouth and jaw to open. This can lead to jaw dislocation and disc injuries that can be associated with cervical myofascial pain, cervical ligament strain, cervical disc protrusion, and upper cervical joint injury (C2, C3). Such whiplash injuries and whiplash headaches are widely disputed in clinical and legal settings.

Headache after head injury may also occur when the soft tissues of the head are injured or when there is scar formation. The site of the injury is often sensitive to finger pressure. Neuralgic headaches may form following local blunt trauma or penetrating scalp injury, resulting in damage to nerve endings. Types of neuralgic headaches include occipital, trigeminal, scalp laceration, and supraorbital neuralgias. Allodynia is represented by hypersensitivity and localised painful sensory disturbances.

There are a number of other reasons for the development of headache disorders following brain injury. It is useful to be observant of medication-overuse headaches and headaches linked to the side effects of other medication. In addition, somatoform headaches, malingering, and pain in association with any somatic or mental health condition should be taken into account.

Finally, it should be noted that patients may have different types of headaches at different times, or a variety of symptoms together which are characteristic of more than one type of headache.

Physiological mechanisms of brain injury and headache

Primary mechanism of brain injury

A number of anatomic structures of the head and neck can be involved in the generation of pain. The pathophysiology of headache following injury to the head, jaw, and neck can be explained with reference to damage to extra-cranial features including bones, arteries, skin, and discs. Lesions causing pain can affect intra-cranial features such as the dura at the brain base, the venous sinuses, and a number of cranial nerves (optic, oculomotor, trigeminal, glossopharyngeal, and vagus). The upper cervical spine, as well as neurological pathways in the spinal cord and brain stem can also contribute to pain generation (Figure 1). A very detailed account of structural and physiological changes following brain injury can be found in Brain Injury Medicine (Zasler, Katz, & Zafonte, 2013).

Example: headache generated by activation of the trigemino-cervical complex

The trigeminal nerve, as one of the major pain transmitting pathways, contains afferent nociceptive fibres from the anterior scalp and cranium, face, mouth, teeth, temporomandibular joints, sinuses, cranial blood vessels, and meninges. The occipital nerves, arising from cervical spinal roots (C2, C3) connect pain stimuli from the posterior head and scalp. Trigeminal and cervical nociceptive neurons merge in the upper cervical spinal cord (also called: the trigemino-cervical complex, Bartsch & Goadsby, 2003). Neurons in this region can perceive afferent pain signals from cervical and trig...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Table of Contents
• LIST OF THERAPY WORKSHEETS
• LIST OF RELAXATION SCRIPTS
• LIST OF QUESTIONNAIRES AND SCORING GUIDELINES
• LIST OF HEADACHE OUTCOMES
• ACKNOWLEDGEMENTS
• ABOUT THE AUTHOR
• SERIES EDITORS’ FOREWORD
• FOREWORD
• INTRODUCTION
• PART I: THEORY
• PART II: PRACTICE
• PART III: THERAPY MANUAL
• APPENDIX I: Therapy worksheets
• APPENDIX II: Relaxation scripts
• APPENDIX III: Questionnaires and scoring guidelines
• APPENDIX IV: Headache outcomes
• REFERENCES
• INDEX